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GENEMEDICS NUTRITION
Author: Dr. George Shanlikian, M.D. | Last Updated: January 31st, 2024
Elampretide, also known as elamipretide or SS-31, is a synthetic tetrapeptide that reduces the production of harmful reactive oxygen species in the body. It works by targeting the cell’s powerhouse known as mitochondria which in turn restores various important cellular processes. Studies show that SS-31 has anti-aging effects that are beneficial for the treatment of age-related diseases, genetic disorders, impaired blood circulation, kidney injury, and heart disease.
The mitochondria are known as the “powerhouse of the cell” as they produce the energy required for various cellular processes. Dysfunctional mitochondria can lead to a wide array of inherited mitochondrial diseases and some age-related diseases. In addition, dysfunctional mitochondria produce abnormally high levels of oxidative factors that can significantly damage cardiolipin, a lipid that plays an integral role in the maintenance of the structural integrity of the mitochondria. By binding to cardiolipin, elampretide protects it from the harmful effects of oxidative stress. This in turn prevents or reduces mitochondrial membrane dysfunction and cell death. In addition, the protective effects of elampretide on the mitochondria help restore various important cellular processes.
Studies show that elampretide (SS-31) can help protect against heart disease via different mechanisms:
SS-31 has also been found to improve cognitive function through its ability to protect the neurons (nerve cells) in the brain:
Evidence also found that SS-31’s antioxidant properties and ability to protect the mitochondria from damage may play a role in preventing cancer:
Studies also show that SS-31 is essential for kidney health:
SS-31 has also been found to treat various forms of lung injury:
Elampretide side effects are very uncommon. There have been some side effects associated with the use of this drug wherein the patient had one of the issues listed below at some point while being on elampretide. However, these side effects weren’t confirmed to be associated with the treatment and could have been a coincidence and not related to the use of elampretide. Despite this, it was listed as a side effect associated with elampretide even though these associated side effects are very uncommon.
Side effects associated with elampretide may include the following:
Chatfield KC, Sparagna GC, Chau S, et al. Elamipretide Improves Mitochondrial Function in the Failing Human Heart. JACC Basic Transl Sci. 2019;4(2):147-157. Published 2019 Apr 29. doi:10.1016/j.jacbts.2018.12.005.
Elamipretide Improves Mitochondrial Function in the Failing Human Heart
The study “Elamipretide Improves Mitochondrial Function in the Failing Human Heart,” conducted by Chatfield KC et al., focuses on the effects of elamipretide, a mitochondrial-targeted therapeutic agent, on mitochondrial and supercomplex function in human hearts with heart failure (HF). The research involved ex vivo treatment of explanted failing and nonfailing ventricular tissue from children and adults with elamipretide. Key findings include significant improvements in oxygen flux and respiratory control ratio in HF samples treated with elamipretide, indicating enhanced mitochondrial function. The study also examined enzyme activities and the effect of HF on tetralinoleoyl cardiolipin, with elamipretide showing beneficial effects in HF hearts.
Read the full article https://www.jacc.org/doi/abs/10.1016/j.jacbts.2018.12.005
Available from https://www.pnas.org/content/117/26/15363
Escribano-Lopez, I., Diaz-Morales, N., Iannantuoni, F. et al. The mitochondrial antioxidant SS-31 increases SIRT1 levels and ameliorates inflammation, oxidative stress and leukocyte-endothelium interactions in type 2 diabetes. Sci Rep 8, 15862 (2018). https://doi.org/10.1038/s41598-018-34251-8
The mitochondrial antioxidant SS-31 increases SIRT1 levels and ameliorates inflammation, oxidative stress and leukocyte-endothelium interactions in type 2 diabetes
In their 2018 study titled “The mitochondrial antioxidant SS-31 increases SIRT1 levels and ameliorates inflammation, oxidative stress, and leukocyte-endothelium interactions in type 2 diabetes,” Escribano-Lopez, I., Diaz-Morales, N., Iannantuoni, F., et al. found that SS-31, a mitochondrial antioxidant, effectively increased SIRT1 levels and offered promising benefits in type 2 diabetes management. The research demonstrated that SS-31 had a positive impact by reducing inflammation and oxidative stress, both common complications in diabetes. Additionally, the antioxidant improved the interactions between white blood cells (leukocytes) and the endothelium within blood vessels, potentially mitigating diabetes-related complications.
Read the full article https://doi.org/10.1038/s41598-018-34251-8
Machiraju P, Wang X, Sabouny R, Huang J, Zhao T, Iqbal F, King M, Prasher D, Lodha A, Jimenez-Tellez N, Ravandi A, Argiropoulos B, Sinasac D, Khan A, Shutt TE and Greenway SC (2019) SS-31 Peptide Reverses the Mitochondrial Fragmentation Present in Fibroblasts From Patients With DCMA, a Mitochondrial Cardiomyopathy. Front. Cardiovasc. Med. 6:167. doi: 10.3389/fcvm.2019.00167.
Shutt TE and Greenway SC (2019) SS-31 Peptide Reverses the Mitochondrial Fragmentation Present in Fibroblasts From Patients With DCMA, a Mitochondrial Cardiomyopathy
The 2019 study titled “SS-31 Peptide Reverses the Mitochondrial Fragmentation Present in Fibroblasts From Patients With DCMA, a Mitochondrial Cardiomyopathy,” conducted by Machiraju P, Wang X, Sabouny R, Huang J, Zhao T, Iqbal F, King M, Prasher D, Lodha A, Jimenez-Tellez N, Ravandi A, Argiropoulos B, Sinasac D, Khan A, Shutt TE, and Greenway SC, investigated the effects of SS-31 peptide on fibroblasts from individuals with DCMA, a mitochondrial cardiomyopathy. The study found that SS-31 peptide was effective in reversing mitochondrial fragmentation in these fibroblasts, suggesting a potential therapeutic benefit for individuals with DCMA.
Read the full article https://www.frontiersin.org/articles/10.3389/fcvm.2019.00167/full
Available from https://jasn.asnjournals.org/content/24/8/1250
Lu HI, Lee FY, Wallace CG, et al. SS31 therapy effectively protects the heart against transverse aortic constriction-induced hypertrophic cardiomyopathy damage. Am J Transl Res. 2017;9(12):5220-5237. Published 2017 Dec 15.
SS31 therapy effectively protects the heart against transverse aortic constriction-induced hypertrophic cardiomyopathy damage
The study conducted by Lu HI, Lee FY, Wallace CG, et al. in 2017, titled “SS31 therapy effectively protects the heart against transverse aortic constriction-induced hypertrophic cardiomyopathy damage,” investigated the therapeutic effects of SS31 therapy in a hypertrophic cardiomyopathy model induced by transverse aortic constriction. The study found that SS31 therapy was effective in protecting the heart against the damage caused by hypertrophic cardiomyopathy. The findings were published in the “American Journal of Translational Research” in December 2017.
Read the full article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5752876/
Liu Y, Yang W, Sun X, Xie L, Yang Y, Sang M, Jiao R. SS31 Ameliorates Sepsis-Induced Heart Injury by Inhibiting Oxidative Stress and Inflammation. Inflammation. 2019 Dec;42(6):2170-2180. doi: 10.1007/s10753-019-01081-3. PMID: 31494795.
SS31 ameliorates sepsis-induced heart injury by inhibiting oxidative stress and inflammation
The 2019 study authored by Liu Y, Yang W, Sun X, Xie L, Yang Y, Sang M, and Jiao R, titled “SS31 Ameliorates Sepsis-Induced Heart Injury by Inhibiting Oxidative Stress and Inflammation,” investigated the effects of SS31 in mitigating heart injury caused by sepsis. The study found that SS31 had a beneficial impact by reducing oxidative stress and inflammation, thus ameliorating heart damage associated with sepsis. The study was published in the journal “Inflammation” in December 2019.
Read the full article https://link.springer.com/article/10.1007/s10753-019-01081-3
Dai DF, Chen T, Szeto H, et al. Mitochondrial targeted antioxidant Peptide ameliorates hypertensive cardiomyopathy. J Am Coll Cardiol. 2011;58(1):73-82. doi:10.1016/j.jacc.2010.12.044.
Mitochondrial Targeted Antioxidant Peptide Ameliorates Hypertensive Cardiomyopathy
The study conducted by Dai DF, Chen T, Szeto H, et al. in 2011, titled “Mitochondrial Targeted Antioxidant Peptide Ameliorates Hypertensive Cardiomyopathy,” investigated the effects of a mitochondrial-targeted antioxidant peptide in improving hypertensive cardiomyopathy. The study found that this antioxidant peptide was effective in ameliorating the condition, potentially by reducing oxidative stress in mitochondria. The research was published in the “Journal of the American College of Cardiology” in January 2011.
Read the full article https://www.jacc.org/doi/abs/10.1016/j.jacc.2010.12.044
Zhang W, Tam J, Shinozaki K, Yin T, Lampe JW, Becker LB, Kim J. Increased Survival Time With SS-31 After Prolonged Cardiac Arrest in Rats. Heart Lung Circ. 2019 Mar;28(3):505-508. doi: 10.1016/j.hlc.2018.01.008. Epub 2018 Feb 7. PMID: 29503242; PMCID: PMC6081272.
Increased Survival Time With SS-31 After Prolonged Cardiac Arrest in Rats
The study by Zhang W, Tam J, Shinozaki K, Yin T, Lampe JW, Becker LB, and Kim J in 2019, titled “Increased Survival Time With SS-31 After Prolonged Cardiac Arrest in Rats,” investigated the effects of SS-31 in prolonging survival time following prolonged cardiac arrest in rats. The study found that SS-31 had a positive impact in extending the survival time of rats subjected to cardiac arrest. This research was published in the “Heart Lung and Circulation” journal in March 2019.
Read the full article https://www.sciencedirect.com/science/article/pii/S1443950618300398
Chavez JD, Tang X, Campbell MD, Reyes G, Kramer PA, Stuppard R, Keller A, Zhang H, Rabinovitch PS, Marcinek DJ, Bruce JE. Mitochondrial protein interaction landscape of SS-31. Proc Natl Acad Sci U S A. 2020 Jun 30;117(26):15363-15373. doi: 10.1073/pnas.2002250117. Epub 2020 Jun 17. PMID: 32554501; PMCID: PMC7334473
Mitochondrial protein interaction landscape of SS-31
The 2020 study authored by Chavez JD, Tang X, Campbell MD, Reyes G, Kramer PA, Stuppard R, Keller A, Zhang H, Rabinovitch PS, Marcinek DJ, and Bruce JE, titled “Mitochondrial Protein Interaction Landscape of SS-31,” explored the interactions between mitochondrial proteins and SS-31, a peptide with mitochondrial-targeted antioxidant properties. The study investigated the protein interaction network associated with SS-31 in mitochondria. This research was published in the “Proceedings of the National Academy of Sciences of the United States of America” (PNAS) in June 2020.
Read the full article https://www.pnas.org/doi/abs/10.1073/pnas.2002250117
Sabbah, H.N., Gupta, R.C., Singh-Gupta, V. et al. Abnormalities of Mitochondrial Dynamics in the Failing Heart: Normalization Following Long-Term Therapy with Elamipretide. Cardiovasc Drugs Ther 32, 319–328 (2018). https://doi.org/10.1007/s10557-018-6805-y
Abnormalities of mitochondrial dynamics in the failing heart: normalization following long-term therapy with elamipretide
The 2018 study conducted by Sabbah H.N., Gupta R.C., Singh-Gupta, V., et al., titled “Abnormalities of Mitochondrial Dynamics in the Failing Heart: Normalization Following Long-Term Therapy with Elamipretide,” investigated the effects of long-term therapy with Elamipretide on mitochondrial dynamics in failing hearts. The study found that there were abnormalities in mitochondrial dynamics in failing hearts, but these abnormalities were normalized following extended treatment with Elamipretide. The research was published in the journal “Cardiovascular Drugs and Therapy.
Read the full article https://link.springer.com/article/10.1007/s10557-018-6805-y
Available from https://www.medrxiv.org/content/10.1101/2020.11.20.20235580v2.full
Available from https://www.ahajournals.org/doi/full/10.1161/circinterventions.117.005487
Available from https://europepmc.org/articles/pmc6588449/bin/nihms1005643-supplement-supplemental_material.pdf
Szeto HH, Liu S, Soong Y, et al. Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1β and IL-18 and Arrests CKD. J Am Soc Nephrol. 2017;28(5):1437-1449. doi:10.1681/ASN.2016070761.
Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1β and IL-18 and Arrests CKD
The 2017 study authored by Szeto HH, Liu S, Soong Y, et al., titled “Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1β and IL-18 and Arrests CKD,” investigated the impact of protecting mitochondria after acute ischemia on the regulation of interleukin-1β (IL-1β) and interleukin-18 (IL-18), as well as its potential role in preventing the progression of chronic kidney disease (CKD). The study found that safeguarding mitochondria post-acute ischemia played a crucial role in preventing the prolonged upregulation of IL-1β and IL-18, ultimately contributing to the arrest of CKD. This research was published in the “Journal of the American Society of Nephrology.”
Read the full article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5407729/
Whitson, J. A., Martín-Pérez, M., Zhang, T., Gaffrey, M. J., Merrihew, G. E., Huang, E., White, C. C., Kavanagh, T. J., Qian, W. J., Campbell, M. D., MacCoss, M. J., Marcinek, D. J., Villén, J., & Rabinovitch, P. S. (2021). Elamipretide (SS-31) treatment attenuates age-associated post-translational modifications of heart proteins. GeroScience, 43(5), 2395–2412. https://doi.org/10.1007/s11357-021-00447-6.
Elamipretide (SS-31) Treatment Attenuates Age-Associated Post-Translational Modifications of Heart Proteins
The 2021 study authored by Whitson, J. A., Martín-Pérez, M., Zhang, T., Gaffrey, M. J., Merrihew, G. E., Huang, E., White, C. C., Kavanagh, T. J., Qian, W. J., Campbell, M. D., MacCoss, M. J., Marcinek, D. J., Villén, J., & Rabinovitch, P. S., titled “Elamipretide (SS-31) Treatment Attenuates Age-Associated Post-Translational Modifications of Heart Proteins,” explored the effects of Elamipretide (SS-31) treatment on age-related post-translational modifications of proteins in the heart. The study found that Elamipretide treatment had a beneficial impact by reducing these age-associated modifications in heart proteins. This research was published in the journal “GeroScience.”
Read the full article https://doi.org/10.1007/s11357-021-00447-6
Rohani, L., Machiraju, P., Sabouny, R., Meng, G., Liu, S., Zhao, T., Iqbal, F., Wang, X., Ravandi, A., Wu, J. C., Khan, A., Shutt, T., Rancourt, D., & Greenway, S. C. (2020). Reversible Mitochondrial Fragmentation in iPSC-Derived Cardiomyocytes From Children With DCMA, a Mitochondrial Cardiomyopathy. The Canadian journal of cardiology, 36(4), 554–563. https://doi.org/10.1016/j.cjca.2019.09.021.
Reversible Mitochondrial Fragmentation in iPSC-Derived Cardiomyocytes From Children With DCMA, a Mitochondrial Cardiomyopathy
The 2020 study authored by Rohani, L., Machiraju, P., Sabouny, R., Meng, G., Liu, S., Zhao, T., Iqbal, F., Wang, X., Ravandi, A., Wu, J. C., Khan, A., Shutt, T., Rancourt, D., & Greenway, S. C., titled “Reversible Mitochondrial Fragmentation in iPSC-Derived Cardiomyocytes From Children With DCMA, a Mitochondrial Cardiomyopathy,” investigated the phenomenon of reversible mitochondrial fragmentation in induced pluripotent stem cell (iPSC)-derived cardiomyocytes obtained from children with DCMA (Dilated Cardiomyopathy with Ataxia). The study focused on understanding the mitochondrial abnormalities associated with DCMA and their potential reversibility. The research was published in “The Canadian Journal of Cardiology.”
Read the full article https://doi.org/10.1016/j.cjca.2019.09.021
Rabinovitch P, Marcinek DJ. THE ROLE OF MITOCHONDRIAL ENERGETICS IN CARDIAC AND SKELETAL MUSCLE AGING. Innov Aging. 2018 Nov 11;2(Suppl 1):348. doi: 10.1093/geroni/igy023.1278. PMCID: PMC6227127.
THE ROLE OF MITOCHONDRIAL ENERGETICS IN CARDIAC AND SKELETAL MUSCLE AGING
The 2018 article authored by Rabinovitch P and Marcinek DJ, titled “The Role of Mitochondrial Energetics in Cardiac and Skeletal Muscle Aging,” discusses the significance of mitochondrial energetics in the aging process of cardiac and skeletal muscle. This article was published in “Innovations in Aging.”
Read the full article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6227127/
Smuder AJ, Roberts BM, Wiggs MP, Kwon OS, Yoo JK, Christou DD, Fuller DD, Szeto HH, Judge AR. Pharmacological targeting of mitochondrial function and reactive oxygen species production prevents colon 26 cancer-induced cardiorespiratory muscle weakness. Oncotarget. 2020 Sep 22;11(38):3502-3514. doi: 10.18632/oncotarget.27748. PMID: 33014286; PMCID: PMC7517961.
Pharmacological targeting of mitochondrial function and reactive oxygen species production prevents colon 26 cancer-induced cardiorespiratory muscle weakness
The study conducted by Smuder AJ, Roberts BM, Wiggs MP, Kwon OS, Yoo JK, Christou DD, Fuller DD, Szeto HH, and Judge AR in 2020, titled “Pharmacological targeting of mitochondrial function and reactive oxygen species production prevents colon 26 cancer-induced cardiorespiratory muscle weakness,” investigated the effects of pharmacological interventions targeting mitochondrial function and reducing reactive oxygen species production in preventing muscle weakness induced by colon 26 cancer. The study found that these interventions were effective in mitigating cancer-induced cardiorespiratory muscle weakness. The research was published in the journal “Oncotarget.”
Read the full article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7517961/
Zhang, H., Alder, N. N., Wang, W., Szeto, H., Marcinek, D. J., & Rabinovitch, P. S. (2020). Reduction of elevated proton leak rejuvenates mitochondria in the aged cardiomyocyte. eLife, 9, e60827. https://doi.org/10.7554/eLife.60827
Reduction of Elevated Proton Leak Rejuvenates Mitochondria in the Aged Cardiomyocyte
The 2020 study authored by Zhang, H., Alder, N. N., Wang, W., Szeto, H., Marcinek, D. J., and Rabinovitch, P. S., titled “Reduction of Elevated Proton Leak Rejuvenates Mitochondria in the Aged Cardiomyocyte,” investigates the rejuvenation of mitochondria in aged cardiomyocytes by reducing elevated proton leak. The study explores the potential benefits of targeting proton leak to improve mitochondrial function in aging heart cells. This research was published in the journal “eLife.”
Read the full article https://doi.org/10.7554/eLife.60827
Available from https://www.ahajournals.org/doi/abs/10.1161/res.125.suppl_1.287
Chiao, Y. A., Zhang, H., Sweetwyne, M., Whitson, J., Ting, Y. S., Basisty, N., Pino, L. K., Quarles, E., Nguyen, N. H., Campbell, M. D., Zhang, T., Gaffrey, M. J., Merrihew, G., Wang, L., Yue, Y., Duan, D., Granzier, H. L., Szeto, H. H., Qian, W. J., Marcinek, D., … Rabinovitch, P. (2020). Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice. eLife, 9, e55513. https://doi.org/10.7554/eLife.55513.
Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice
The 2020 study authored by Chiao, Y. A., Zhang, H., Sweetwyne, M., Whitson, J., Ting, Y. S., Basisty, N., Pino, L. K., Quarles, E., Nguyen, N. H., Campbell, M. D., Zhang, T., Gaffrey, M. J., Merrihew, G., Wang, L., Yue, Y., Duan, D., Granzier, H. L., Szeto, H. H., Qian, W. J., Marcinek, D., and Rabinovitch, P., titled “Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice,” investigates the reversal of cardiac dysfunction in aged mice through the restoration of mitochondrial function in late life. The study explores the potential benefits of rejuvenating mitochondria in old age to improve heart function. This research was published in the journal “eLife.”
Read the full article https://doi.org/10.7554/eLife.55513
Whitson JA, Bitto A, Zhang H, Sweetwyne MT, Coig R, Bhayana S, Shankland EG, Wang L, Bammler TK, Mills KF, Imai SI, Conley KE, Marcinek DJ, Rabinovitch PS. SS-31 and NMN: Two paths to improve metabolism and function in aged hearts. Aging Cell. 2020 Oct;19(10):e13213. doi: 10.1111/acel.13213. Epub 2020 Aug 11. PMID: 32779818; PMCID: PMC7576234.
SS-31 and NMN: Two paths to improve metabolism and function in aged hearts
The 2020 study authored by Whitson JA, Bitto A, Zhang H, Sweetwyne MT, Coig R, Bhayana S, Shankland EG, Wang L, Bammler TK, Mills KF, Imai SI, Conley KE, Marcinek DJ, and Rabinovitch PS, titled “SS-31 and NMN: Two paths to improve metabolism and function in aged hearts,” investigates two different approaches, SS-31 and NMN (nicotinamide mononucleotide), to enhance metabolism and function in aging hearts. The study explores the potential benefits of these interventions in improving heart health in aging individuals. This research was published in the journal “Aging Cell.”
Read the full article https://onlinelibrary.wiley.com/doi/abs/10.1111/acel.13213
Whitson, J. A., Johnson, R., Wang, L., Bammler, T. K., Imai, S. I., Zhang, H., Fredrickson, J., Latorre-Esteves, E., Bitto, A., MacCoss, M. J., & Rabinovitch, P. S. (2022). Age-related disruption of the proteome and acetylome in mouse hearts is associated with loss of function and attenuated by elamipretide (SS-31) and nicotinamide mononucleotide (NMN) treatment. GeroScience, 44(3), 1621–1639. https://doi.org/10.1007/s11357-022-00564-w.
Age-related disruption of the proteome and acetylome in mouse hearts is associated with loss of function and attenuated by elamipretide (SS-31) and nicotinamide mononucleotide (NMN) treatment
The 2022 study authored by Whitson, J. A., Johnson, R., Wang, L., Bammler, T. K., Imai, S. I., Zhang, H., Fredrickson, J., Latorre-Esteves, E., Bitto, A., MacCoss, M. J., and Rabinovitch, P. S., titled “Age-related disruption of the proteome and acetylome in mouse hearts is associated with loss of function and attenuated by elamipretide (SS-31) and nicotinamide mononucleotide (NMN) treatment,” examines the impact of aging on the proteome and acetylome of mouse hearts, along with its association with the loss of cardiac function. The study investigates how treatment with elamipretide (SS-31) and nicotinamide mononucleotide (NMN) can potentially mitigate these age-related disruptions in heart health.
Read the full article https://doi.org/10.1007/s11357-022-00564-w
Sabbah, H. N., Gupta, R. C., Kohli, S., Wang, M., Hachem, S., & Zhang, K. (2016). Chronic Therapy With Elamipretide (MTP-131), a Novel Mitochondria-Targeting Peptide, Improves Left Ventricular and Mitochondrial Function in Dogs With Advanced Heart Failure. Circulation. Heart failure, 9(2), e002206. https://doi.org/10.1161/CIRCHEARTFAILURE.115.002206.
Chronic Therapy With Elamipretide (MTP-131), a Novel Mitochondria-Targeting Peptide, Improves Left Ventricular and Mitochondrial Function in Dogs With Advanced Heart Failure
The 2016 study authored by Sabbah, H. N., Gupta, R. C., Kohli, S., Wang, M., Hachem, S., and Zhang, K., titled “Chronic Therapy With Elamipretide (MTP-131), a Novel Mitochondria-Targeting Peptide, Improves Left Ventricular and Mitochondrial Function in Dogs With Advanced Heart Failure,” examines the effects of chronic treatment with Elamipretide (MTP-131), a mitochondria-targeting peptide, on left ventricular function and mitochondrial function in dogs suffering from advanced heart failure. The study found that this therapy led to improvements in both left ventricular and mitochondrial function in these dogs. This research was published in “Circulation: Heart Failure.”
Read the full article https://doi.org/10.1161/CIRCHEARTFAILURE.115.002206
Sabbah HN, Gupta RC, Singh-Gupta V, Zhang K. Effects of elamipretide on skeletal muscle in dogs with experimentally induced heart failure. ESC Heart Fail. 2019 Apr;6(2):328-335. doi: 10.1002/ehf2.12408. Epub 2019 Jan 28. PMID: 30688415; PMCID: PMC6437430.
Effects of elamipretide on skeletal muscle in dogs with experimentally induced heart failure
The 2019 study authored by Sabbah HN, Gupta RC, Singh-Gupta V, and Zhang K, titled “Effects of elamipretide on skeletal muscle in dogs with experimentally induced heart failure,” investigates the impact of elamipretide on skeletal muscle in dogs that have experimentally induced heart failure. The study examines how elamipretide treatment affects the skeletal muscle function in this context. This research was published in “ESC Heart Failure.”
Read the full article https://onlinelibrary.wiley.com/doi/abs/10.1002/ehf2.12408
Allen, M. E., Pennington, E. R., Perry, J. B., Dadoo, S., Makrecka-Kuka, M., Dambrova, M., Moukdar, F., Patel, H. D., Han, X., Kidd, G. K., Benson, E. K., Raisch, T. B., Poelzing, S., Brown, D. A., & Shaikh, S. R. (2020). The cardiolipin-binding peptide elamipretide mitigates fragmentation of cristae networks following cardiac ischemia reperfusion in rats. Communications biology, 3(1), 389. https://doi.org/10.1038/s42003-020-1101-3.
The cardiolipin-binding peptide elamipretide mitigates fragmentation of cristae networks following cardiac ischemia reperfusion in rats
The 2020 study authored by Allen, M. E., Pennington, E. R., Perry, J. B., Dadoo, S., Makrecka-Kuka, M., Dambrova, M., Moukdar, F., Patel, H. D., Han, X., Kidd, G. K., Benson, E. K., Raisch, T. B., Poelzing, S., Brown, D. A., and Shaikh, S. R., titled “The cardiolipin-binding peptide elamipretide mitigates fragmentation of cristae networks following cardiac ischemia reperfusion in rats,” investigates the impact of the cardiolipin-binding peptide elamipretide on mitigating the fragmentation of cristae networks in the mitochondria following cardiac ischemia-reperfusion in rats. The study explores the potential benefits of elamipretide in preserving mitochondrial structure and function in this context. This research was published in “Communications Biology.”
Read the full article https://www.nature.com/articles/s42003-020-1101-3
Reid Thompson, W., Hornby, B., Manuel, R., Bradley, E., Laux, J., Carr, J., & Vernon, H. J. (2021). A phase 2/3 randomized clinical trial followed by an open-label extension to evaluate the effectiveness of elamipretide in Barth syndrome, a genetic disorder of mitochondrial cardiolipin metabolism. Genetics in medicine : official journal of the American College of Medical Genetics, 23(3), 471–478. https://doi.org/10.1038/s41436-020-01006-8.
A phase 2/3 randomized clinical trial followed by an open-label extension to evaluate the effectiveness of elamipretide in Barth syndrome, a genetic disorder of mitochondrial cardiolipin metabolism.
The 2021 study authored by Reid Thompson, W., Hornby, B., Manuel, R., Bradley, E., Laux, J., Carr, J., and Vernon, H. J., titled “A phase 2/3 randomized clinical trial followed by an open-label extension to evaluate the effectiveness of elamipretide in Barth syndrome, a genetic disorder of mitochondrial cardiolipin metabolism,” reports on a clinical trial that aimed to evaluate the effectiveness of elamipretide in individuals with Barth syndrome, a genetic disorder associated with mitochondrial cardiolipin metabolism. The study involved a phase 2/3 randomized clinical trial followed by an open-label extension to assess the potential benefits of elamipretide in treating this rare genetic disorder. This research was published in “Genetics in Medicine,” the official journal of the American College of Medical Genetics.
Read the full article https://doi.org/10.1038/s41436-020-01006-8
Campbell, M. D., Duan, J., Samuelson, A. T., Gaffrey, M. J., Merrihew, G. E., Egertson, J. D., Wang, L., Bammler, T. K., Moore, R. J., White, C. C., Kavanagh, T. J., Voss, J. G., Szeto, H. H., Rabinovitch, P. S., MacCoss, M. J., Qian, W. J., & Marcinek, D. J. (2019). Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice. Free radical biology & medicine, 134, 268–281. https://doi.org/10.1016/j.freeradbiomed.2018.12.031.
Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice
The 2019 study authored by Campbell, M. D., Duan, J., Samuelson, A. T., Gaffrey, M. J., Merrihew, G. E., Egertson, J. D., Wang, L., Bammler, T. K., Moore, R. J., White, C. C., Kavanagh, T. J., Voss, J. G., Szeto, H. H., Rabinovitch, P. S., MacCoss, M. J., Qian, W. J., and Marcinek, D. J., titled “Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice,” explores the effects of SS-31, a mitochondria-targeted antioxidant peptide, on improving mitochondrial function and exercise tolerance in aging mice. The study investigates how SS-31 can potentially reverse age-related redox stress and enhance the ability to engage in physical activity among older mice. This research was published in “Free Radical Biology & Medicine.”
Read the full article https://doi.org/10.1016/j.freeradbiomed.2018.12.031
Jia YL, Sun SJ, Chen JH, Jia Q, Huo TT, Chu LF, Bai JT, Yu YJ, Yan XX, Wang JH. SS31, a Small Molecule Antioxidant Peptide, Attenuates β-Amyloid Elevation, Mitochondrial/Synaptic Deterioration and Cognitive Deficit in SAMP8 Mice. Curr Alzheimer Res. 2016;13(3):297-306. doi: 10.2174/1567205013666151218150004. PMID: 26679857.
SS31, a Small Molecule Antioxidant Peptide, Attenuates β-Amyloid Elevation, Mitochondrial/Synaptic Deterioration and Cognitive Deficit in SAMP8 Mice
The 2016 study authored by Jia YL, Sun SJ, Chen JH, Jia Q, Huo TT, Chu LF, Bai JT, Yu YJ, Yan XX, and Wang JH, titled “SS31, a Small Molecule Antioxidant Peptide, Attenuates β-Amyloid Elevation, Mitochondrial/Synaptic Deterioration and Cognitive Deficit in SAMP8 Mice,” explores the effects of SS31, a small molecule antioxidant peptide, on mitigating β-amyloid elevation, mitochondrial and synaptic deterioration, as well as cognitive deficits in SAMP8 mice. The study investigates the potential neuroprotective and cognitive-enhancing properties of SS31 in the context of Alzheimer’s disease. This research was published in “Current Alzheimer Research.”
Read the full article https://www.ingentaconnect.com/content/ben/car/2016/00000013/00000003/art00011
Wu J, Hao S, Sun XR, et al. Elamipretide (SS-31) Ameliorates Isoflurane-Induced Long-Term Impairments of Mitochondrial Morphogenesis and Cognition in Developing Rats. Front Cell Neurosci. 2017;11:119. Published 2017 Apr 25. doi:10.3389/fncel.2017.00119.
Elamipretide (SS-31) Ameliorates Isoflurane-Induced Long-Term Impairments of Mitochondrial Morphogenesis and Cognition in Developing Rats
The 2017 study authored by Wu J, Hao S, Sun XR, et al., titled “Elamipretide (SS-31) Ameliorates Isoflurane-Induced Long-Term Impairments of Mitochondrial Morphogenesis and Cognition in Developing Rats,” investigates the potential benefits of elamipretide (SS-31) in mitigating long-term impairments in mitochondrial morphogenesis and cognition induced by isoflurane exposure in developing rats. The study explores the effects of elamipretide on mitigating the adverse consequences of anesthesia exposure during development. This research was published in “Frontiers in Cellular Neuroscience.”
Read the full article https://www.frontiersin.org/articles/10.3389/fncel.2017.00119/full
Wu, J., Zhang, M., Li, H., Sun, X., Hao, S., Ji, M., Yang, J., & Li, K. (2016). BDNF pathway is involved in the protective effects of SS-31 on isoflurane-induced cognitive deficits in aging mice. Behavioural brain research, 305, 115–121. https://doi.org/10.1016/j.bbr.2016.02.036.
BDNF pathway is involved in the protective effects of SS-31 on isoflurane-induced cognitive deficits in aging mice
The 2016 study authored by Wu, J., Zhang, M., Li, H., Sun, X., Hao, S., Ji, M., Yang, J., and Li, K., titled “BDNF Pathway is Involved in the Protective Effects of SS-31 on Isoflurane-Induced Cognitive Deficits in Aging Mice,” investigates the role of the brain-derived neurotrophic factor (BDNF) pathway in the protective effects of SS-31 against isoflurane-induced cognitive deficits in aging mice. The study explores the potential involvement of the BDNF pathway in mediating the cognitive benefits of SS-31 in the context of anesthesia-induced cognitive impairment in older mice. This research was published in “Behavioural Brain Research.”
Read the full article https://doi.org/10.1016/j.bbr.2016.02.036
Tarantini, S, Valcarcel‐Ares, NM, Yabluchanskiy, A, et al. Treatment with the mitochondrial‐targeted antioxidant peptide SS‐31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice. Aging Cell. 2018; 17:e12731. https://doi.org/10.1111/acel.12731.
Treatment with the mitochondrial‐targeted antioxidant peptide SS‐31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice
The 2018 study authored by Tarantini, S, Valcarcel‐Ares, NM, Yabluchanskiy, A, et al., titled “Treatment with the mitochondrial‐targeted antioxidant peptide SS‐31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice,” investigates the impact of treatment with the mitochondrial-targeted antioxidant peptide SS-31 on neurovascular coupling responses, cerebrovascular endothelial function, and cognitive function in aged mice. The study explores the potential cognitive and vascular benefits of SS-31 in the context of aging. This research was published in “Aging Cell.”
Read the full article https://doi.org/10.1111/acel.12731
Zhao, W., Xu, Z., Cao, J. et al. Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic and memory impairment induced by lipopolysaccharide in mice. J Neuroinflammation 16, 230 (2019). https://doi.org/10.1186/s12974-019-1627-9.
Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic and memory impairment induced by lipopolysaccharide in mice
The 2019 study authored by Zhao, W., Xu, Z., Cao, J., et al., titled “Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic and memory impairment induced by lipopolysaccharide in mice,” investigates the effects of Elamipretide (SS-31) on mitigating mitochondrial dysfunction, synaptic impairment, and memory deficits induced by lipopolysaccharide in mice. The study explores the potential neuroprotective and cognitive-enhancing properties of Elamipretide in the context of inflammation-induced neurological impairments. This research was published in the journal “Journal of Neuroinflammation.”
Read the full article https://doi.org/10.1186/s12974-019-1627-9
Tarantini, S., Valcarcel-Ares, N. M., Yabluchanskiy, A., Fulop, G. A., Hertelendy, P., Gautam, T., Farkas, E., Perz, A., Rabinovitch, P. S., Sonntag, W. E., Csiszar, A., & Ungvari, Z. (2018). Treatment with the mitochondrial-targeted antioxidant peptide SS-31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice. Aging cell, 17(2), e12731. https://doi.org/10.1111/acel.12731.
Treatment with the mitochondrial-targeted antioxidant peptide SS-31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice.
The 2018 study authored by Tarantini, S., Valcarcel-Ares, N. M., Yabluchanskiy, A., Fulop, G. A., Hertelendy, P., Gautam, T., Farkas, E., Perz, A., Rabinovitch, P. S., Sonntag, W. E., Csiszar, A., & Ungvari, Z., titled “Treatment with the mitochondrial-targeted antioxidant peptide SS-31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice,” investigates the effects of treatment with the mitochondrial-targeted antioxidant peptide SS-31 on neurovascular coupling responses, cerebrovascular endothelial function, and cognitive function in aged mice. The study explores the potential benefits of SS-31 in improving cerebrovascular health and cognitive performance in aging mice. This research was published in the journal “Aging Cell.”
Read the full article https://doi.org/10.1111/acel.12731
Liu, Y., Fu, H., Wu, Y., Nie, B., Liu, F., Wang, T., Xiao, W., Yang, S., Kan, M., & Fan, L. (2021). Elamipretide (SS-31) Improves Functional Connectivity in Hippocampus and Other Related Regions Following Prolonged Neuroinflammation Induced by Lipopolysaccharide in Aged Rats. Frontiers in aging neuroscience, 13, 600484. https://doi.org/10.3389/fnagi.2021.600484.
Elamipretide (SS-31) Improves Functional Connectivity in Hippocampus and Other Related Regions Following Prolonged Neuroinflammation Induced by Lipopolysaccharide in Aged Rats
The 2021 study authored by Liu, Y., Fu, H., Wu, Y., Nie, B., Liu, F., Wang, T., Xiao, W., Yang, S., Kan, M., & Fan, L., titled “Elamipretide (SS-31) Improves Functional Connectivity in Hippocampus and Other Related Regions Following Prolonged Neuroinflammation Induced by Lipopolysaccharide in Aged Rats,” investigates the effects of Elamipretide (SS-31) on improving functional connectivity in the hippocampus and other related brain regions following prolonged neuroinflammation induced by lipopolysaccharide in aged rats. The study explores the potential benefits of SS-31 in enhancing brain function and connectivity in the context of neuroinflammatory conditions associated with aging. This research was published in the journal “Frontiers in Aging Neuroscience.”
Read the full article https://doi.org/10.3389/fnagi.2021.600484
Zuo, Y., Yin, L., Cheng, X., Li, J., Wu, H., Liu, X., Gu, E., & Wu, J. (2020). Elamipretide Attenuates Pyroptosis and Perioperative Neurocognitive Disorders in Aged Mice. Frontiers in cellular neuroscience, 14, 251. https://doi.org/10.3389/fncel.2020.00251.
Elamipretide Attenuates Pyroptosis and Perioperative Neurocognitive Disorders in Aged Mice
The 2020 study authored by Zuo, Y., Yin, L., Cheng, X., Li, J., Wu, H., Liu, X., Gu, E., & Wu, J., titled “Elamipretide Attenuates Pyroptosis and Perioperative Neurocognitive Disorders in Aged Mice,” investigates the effects of Elamipretide on attenuating pyroptosis and perioperative neurocognitive disorders in aged mice. The study explores the potential benefits of Elamipretide in protecting against cognitive impairment and inflammatory processes during the perioperative period in aged mice. This research was published in the journal “Frontiers in Cellular Neuroscience.”
Read the full article https://doi.org/10.3389/fncel.2020.00251
Czigler, A., Toth, L., Szarka, N., Berta, G., Amrein, K., Czeiter, E., Lendvai-Emmert, D., Bodo, K., Tarantini, S., Koller, A., Ungvari, Z., Buki, A., & Toth, P. (2019). Hypertension Exacerbates Cerebrovascular Oxidative Stress Induced by Mild Traumatic Brain Injury: Protective Effects of the Mitochondria-Targeted Antioxidative Peptide SS-31. Journal of neurotrauma, 36(23), 3309–3315. https://doi.org/10.1089/neu.2019.6439
Hypertension Exacerbates Cerebrovascular Oxidative Stress Induced by Mild Traumatic Brain Injury: Protective Effects of the Mitochondria-Targeted Antioxidative Peptide SS-31
The 2019 study authored by Czigler, A., Toth, L., Szarka, N., Berta, G., Amrein, K., Czeiter, E., Lendvai-Emmert, D., Bodo, K., Tarantini, S., Koller, A., Ungvari, Z., Buki, A., and Toth, P., titled “Hypertension Exacerbates Cerebrovascular Oxidative Stress Induced by Mild Traumatic Brain Injury: Protective Effects of the Mitochondria-Targeted Antioxidative Peptide SS-31,” investigates the impact of hypertension on cerebrovascular oxidative stress induced by mild traumatic brain injury and explores the potential protective effects of the mitochondria-targeted antioxidative peptide SS-31 in this context. The study assesses whether SS-31 can mitigate oxidative stress and its detrimental effects on cerebrovascular function following mild traumatic brain injury in hypertensive individuals. This research was published in the “Journal of Neurotrauma.”
Read the full article https://doi.org/10.1089/neu.2019.6439
Yang, L., Zhao, K., Calingasan, N. Y., Luo, G., Szeto, H. H., & Beal, M. F. (2009). Mitochondria targeted peptides protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity. Antioxidants & redox signaling, 11(9), 2095–2104. https://doi.org/10.1089/ars.2009.2445.
Mitochondria targeted peptides protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity
The 2009 study authored by Yang, L., Zhao, K., Calingasan, N. Y., Luo, G., Szeto, H. H., and Beal, M. F., titled “Mitochondria targeted peptides protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity,” investigates the protective effects of mitochondria-targeted peptides against the neurotoxicity induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The study explores whether these peptides can protect against neurodegenerative damage caused by MPTP, a compound known to induce Parkinson’s disease-like symptoms in experimental models. This research was published in the “Antioxidants & Redox Signaling” journal.
Read the full article https://doi.org/10.1089/ars.2009.2445
Reddy, P. H., Manczak, M., Yin, X., & Reddy, A. P. (2018). Synergistic Protective Effects of Mitochondrial Division Inhibitor 1 and Mitochondria-Targeted Small Peptide SS31 in Alzheimer’s Disease. Journal of Alzheimer’s disease : JAD, 62(4), 1549–1565. https://doi.org/10.3233/JAD-170988.
Synergistic Protective Effects of Mitochondrial Division Inhibitor 1 and Mitochondria-Targeted Small Peptide SS31 in Alzheimer’s Disease
The 2018 study authored by Reddy, P. H., Manczak, M., Yin, X., and Reddy, A. P., titled “Synergistic Protective Effects of Mitochondrial Division Inhibitor 1 and Mitochondria-Targeted Small Peptide SS31 in Alzheimer’s Disease,” investigates the synergistic protective effects of Mitochondrial Division Inhibitor 1 and the mitochondria-targeted small peptide SS31 in Alzheimer’s disease. The study explores the potential benefits of these compounds in protecting against Alzheimer’s disease-related pathological changes and neurodegeneration. This research was published in the “Journal of Alzheimer’s Disease.”
Read the full article https://doi.org/10.3233/JAD-170988
Mo, Y., Deng, S., Zhang, L., Huang, Y., Li, W., Peng, Q., Liu, Z., & Ai, Y. (2019). SS-31 reduces inflammation and oxidative stress through the inhibition of Fis1 expression in lipopolysaccharide-stimulated microglia. Biochemical and biophysical research communications, 520(1), 171–178. https://doi.org/10.1016/j.bbrc.2019.09.077.
SS-31 reduces inflammation and oxidative stress through the inhibition of Fis1 expression in lipopolysaccharide-stimulated microglia
This reference you’ve provided is for a scientific article titled “SS-31 reduces inflammation and oxidative stress through the inhibition of Fis1 expression in lipopolysaccharide-stimulated microglia.” It was authored by Mo, Y., Deng, S., Zhang, L., Huang, Y., Li, W., Peng, Q., Liu, Z., & Ai, Y., and published in the journal “Biochemical and Biophysical Research Communications” in 2019.
The study focuses on SS-31, a peptide known for its potential in treating various diseases related to oxidative stress and mitochondrial dysfunction. The research specifically examines the effect of SS-31 on microglia, which are a type of glial cell located throughout the brain and spinal cord. Microglia are known to be involved in inflammatory responses and oxidative stress within the central nervous system.
Read the full article https://www.sciencedirect.com/science/article/pii/S0006291X19318042
Nhu NT, Xiao SY, Liu Y, Kumar VB, Cui ZY, Lee SD. Neuroprotective Effects of a Small Mitochondrially-Targeted Tetrapeptide Elamipretide in Neurodegeneration. Front Integr Neurosci. 2022 Jan 17;15:747901. doi: 10.3389/fnint.2021.747901. PMID: 35111001; PMCID: PMC8801496.
Neuroprotective Effects of a Small Mitochondrially-Targeted Tetrapeptide Elamipretide in Neurodegeneration
The reference you provided is for a scientific article titled “Neuroprotective Effects of a Small Mitochondrially-Targeted Tetrapeptide Elamipretide in Neurodegeneration.” This study was authored by Nhu NT, Xiao SY, Liu Y, Kumar VB, Cui ZY, Lee SD and published in the journal “Frontiers in Integrative Neuroscience” in January 2022.
Elamipretide, previously known as SS-31, is a small tetrapeptide that has been the focus of research due to its potential in treating various conditions related to mitochondrial dysfunction. This particular study explores the neuroprotective effects of elamipretide in the context of neurodegenerative diseases.
Neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and Huntington’s disease, are characterized by the progressive loss of structure and function of neurons. Mitochondrial dysfunction is a common feature in these diseases, leading to issues such as energy deficits, increased oxidative stress, and cell death.
Read the full article https://www.frontiersin.org/articles/10.3389/fnint.2021.747901/full
Smuder AJ, Roberts BM, Wiggs MP, Kwon OS, Yoo JK, Christou DD, Fuller DD, Szeto HH, Judge AR. Pharmacological targeting of mitochondrial function and reactive oxygen species production prevents colon 26 cancer-induced cardiorespiratory muscle weakness. Oncotarget. 2020 Sep 22;11(38):3502-3514. doi: 10.18632/oncotarget.27748. PMID: 33014286; PMCID: PMC7517961.
Pharmacological targeting of mitochondrial function and reactive oxygen species production prevents colon 26 cancer-induced cardiorespiratory muscle weakness
The reference you provided is for a scientific article titled “Pharmacological targeting of mitochondrial function and reactive oxygen species production prevents colon 26 cancer-induced cardiorespiratory muscle weakness.” This study was authored by Smuder AJ, Roberts BM, Wiggs MP, Kwon OS, Yoo JK, Christou DD, Fuller DD, Szeto HH, Judge AR and published in the journal “Oncotarget” in September 2020.
This research focuses on the impact of colon cancer (specifically, a model using colon 26 cancer cells) on the strength and functionality of cardiorespiratory muscles. The study particularly explores how cancer progression leads to muscle weakness, a common and debilitating symptom experienced by many cancer patients.
Read the full article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7517961/
Wang B, Fu J, Yu T, Xu A, Qin W, Yang Z, Chen Y, Wang H. Contradictory effects of mitochondria- and non-mitochondria-targeted antioxidants on hepatocarcinogenesis by altering DNA repair in mice. Hepatology. 2018 Feb;67(2):623-635. doi: 10.1002/hep.29518. Epub 2018 Jan 7. PMID: 28898446.
Contradictory effects of mitochondria- and non-mitochondria-targeted antioxidants on hepatocarcinogenesis by altering DNA repair in mice
The reference you’ve provided is to a scientific article titled “Contradictory effects of mitochondria- and non-mitochondria-targeted antioxidants on hepatocarcinogenesis by altering DNA repair in mice.” Authored by Wang B, Fu J, Yu T, Xu A, Qin W, Yang Z, Chen Y, Wang H, this study was published in the journal “Hepatology” in February 2018.
This research investigates the effects of antioxidants that are targeted either specifically at mitochondria or those that have a broader, non-mitochondria-specific target, in the context of liver cancer development (hepatocarcinogenesis) in mice. The study particularly focuses on how these different types of antioxidants influence DNA repair mechanisms, which play a crucial role in preventing cancer.
Read the full article https://aasldpubs.onlinelibrary.wiley.com/doi/abs/10.1002/hep.29518
Chavez JD, Tang X, Campbell MD, Reyes G, Kramer PA, Stuppard R, Keller A, Zhang H, Rabinovitch PS, Marcinek DJ, Bruce JE. Mitochondrial protein interaction landscape of SS-31. Proc Natl Acad Sci U S A. 2020 Jun 30;117(26):15363-15373. doi: 10.1073/pnas.2002250117. Epub 2020 Jun 17. PMID: 32554501; PMCID: PMC7334473.
Mitochondrial protein interaction landscape of SS-31
The reference you provided is for a scientific article titled “Mitochondrial protein interaction landscape of SS-31.” Authored by Chavez JD, Tang X, Campbell MD, Reyes G, Kramer PA, Stuppard R, Keller A, Zhang H, Rabinovitch PS, Marcinek DJ, Bruce JE, this study was published in the “Proceedings of the National Academy of Sciences of the United States of America (PNAS)” in June 2020.
SS-31, also known as elamipretide, is a peptide that has garnered significant interest due to its potential therapeutic effects, particularly in the context of mitochondrial dysfunction. This study specifically investigates the interaction landscape of SS-31 with mitochondrial proteins.
Understanding how SS-31 interacts with mitochondrial proteins is crucial for comprehending its mechanism of action at a molecular level. Mitochondria are vital organelles in cells, responsible for energy production and playing roles in various cellular processes, including cell death and signaling. Dysfunctional mitochondria are implicated in a range of diseases, from metabolic disorders to neurodegenerative diseases.
Read the full article https://www.pnas.org/doi/abs/10.1073/pnas.2002250117
Ma W, Zhu X, Ding X, et al. Protective effects of SS31 on t‑BHP induced oxidative damage in 661W cells. Mol Med Rep. 2015;12(4):5026-5034. doi:10.3892/mmr.2015.4055.
Protective effects of SS31 on t‑BHP induced oxidative damage in 661W cells
The reference you’ve provided is for a scientific article titled “Protective effects of SS31 on t-BHP induced oxidative damage in 661W cells,” authored by Ma W, Zhu X, Ding X, et al. This study was published in the journal “Molecular Medicine Reports” in 2015.
In this study, the authors explore the protective effects of SS31, a mitochondria-targeted peptide, against oxidative damage in 661W cells. The 661W cell line is commonly used as a model for studying retinal cells, particularly in the context of retinal degenerative diseases.
The oxidative damage in this study is induced by tert-butyl hydroperoxide (t-BHP), a compound known to generate reactive oxygen species (ROS) and cause oxidative stress in cells. Oxidative stress is a state where there’s an imbalance between the production of ROS and the ability of the body to counteract or detoxify their harmful effects. It’s a common contributing factor in many diseases, including neurodegenerative diseases and conditions related to retinal degeneration.
Read the full article https://www.spandidos-publications.com/10.3892/mmr.2015.4055
Ballarò, R., Lopalco, P., Audrito, V., Beltrà, M., Pin, F., Angelini, R., Costelli, P., Corcelli, A., Bonetto, A., Szeto, H. H., O’Connell, T. M., & Penna, F. (2021). Targeting Mitochondria by SS-31 Ameliorates the Whole Body Energy Status in Cancer- and Chemotherapy-Induced Cachexia. Cancers, 13(4), 850. https://doi.org/10.3390/cancers13040850
Targeting Mitochondria by SS-31 Ameliorates the Whole Body Energy Status in Cancer- and Chemotherapy-Induced Cachexia
The reference you provided is for a scientific article titled “Targeting Mitochondria by SS-31 Ameliorates the Whole Body Energy Status in Cancer- and Chemotherapy-Induced Cachexia.” Authored by Ballarò, R., Lopalco, P., Audrito, V., Beltrà, M., Pin, F., Angelini, R., Costelli, P., Corcelli, A., Bonetto, A., Szeto, H. H., O’Connell, T. M., & Penna, F., this study was published in the journal “Cancers” in 2021.
Cachexia is a complex syndrome associated with chronic diseases like cancer, characterized by severe body weight, muscle, and fat loss. It is a significant cause of morbidity and mortality in cancer patients, often exacerbated by chemotherapy. A key component of cachexia is the altered energy metabolism in the body.
SS-31, also known as elamipretide, is a peptide that specifically targets mitochondria. It has been shown to have potential therapeutic benefits in various conditions related to mitochondrial dysfunction. The mitochondrial dysfunction is often a contributing factor in the altered metabolism observed in cachexia.
Read the full article https://www.mdpi.com/2072-6694/13/4/850
Beltrà, M., Pin, F., Ballarò, R., Costelli, P., & Penna, F. (2021). Mitochondrial Dysfunction in Cancer Cachexia: Impact on Muscle Health and Regeneration. Cells, 10(11), 3150. https://doi.org/10.3390/cells10113150
Mitochondrial Dysfunction in Cancer Cachexia: Impact on Muscle Health and Regeneration
The reference you’ve provided is for a scientific article titled “Mitochondrial Dysfunction in Cancer Cachexia: Impact on Muscle Health and Regeneration.” Authored by Beltrà, M., Pin, F., Ballarò, R., Costelli, P., & Penna, F., this study was published in the journal “Cells” in 2021.
Cancer cachexia is a complex metabolic syndrome associated with underlying cancer, characterized by severe loss of muscle mass and often weight loss, including both fat and muscle tissue. This condition significantly impacts the quality of life and prognosis of cancer patients.
One of the critical aspects explored in this study is the role of mitochondrial dysfunction in cancer cachexia, particularly focusing on its impact on muscle health and regeneration. Mitochondria are crucial for energy production in cells and play a vital role in muscle function and repair. In the context of cancer cachexia, mitochondrial dysfunction can contribute to muscle wasting and weakness, exacerbating the condition.
Read the full article https://www.mdpi.com/2073-4409/10/11/3150?trk=public_post_main-feed-card-text
Available from https://www.sciencedirect.com/science/article/pii/S0753332220307149.
Wyss J-C, Kumar R, Mikulic J, Schneider M, Mary J-L, Aebi JD, Juillerat-Jeanneret L and Golshayan D (2019) Differential Effects of the Mitochondria-Active Tetrapeptide SS-31 (D-Arg-dimethylTyr-Lys-Phe-NH2) and Its Peptidase-Targeted Prodrugs in Experimental Acute Kidney Injury. Front. Pharmacol. 10:1209. doi: 10.3389/fphar.2019.01209.
Differential Effects of the Mitochondria-Active Tetrapeptide SS-31 (D-Arg-dimethylTyr-Lys-Phe-NH2) and Its Peptidase-Targeted Prodrugs in Experimental Acute Kidney Injury.
The article titled “Differential Effects of the Mitochondria-Active Tetrapeptide SS-31 (D-Arg-dimethylTyr-Lys-Phe-NH2) and Its Peptidase-Targeted Prodrugs in Experimental Acute Kidney Injury” by Wyss J-C, Kumar R, Mikulic J, Schneider M, Mary J-L, Aebi JD, Juillerat-Jeanneret L, and Golshayan D, published in “Frontiers in Pharmacology” in 2019, explores the effects of SS-31 and its prodrugs on acute kidney injury (AKI). This study is significant for understanding the potential therapeutic applications of SS-31, particularly in the context of kidney diseases. The focus on both the peptide and its prodrugs provides insights into their respective efficacies and mechanisms of action in treating or mitigating AKI.
Read the full article https://www.frontiersin.org/articles/10.3389/fphar.2019.01209/full
Available from https://journals.physiology.org/doi/full/10.1152/ajprenal.00395.2007
Mizuguchi, Y., Chen, J., Seshan, S. V., Poppas, D. P., Szeto, H. H., & Felsen, D. (2008). A novel cell-permeable antioxidant peptide decreases renal tubular apoptosis and damage in unilateral ureteral obstruction. American journal of physiology. Renal physiology, 295(5), F1545–F1553. https://doi.org/10.1152/ajprenal.00395.2007.
A novel cell-permeable antioxidant peptide decreases renal tubular apoptosis and damage in unilateral ureteral obstruction
The article “A novel cell-permeable antioxidant peptide decreases renal tubular apoptosis and damage in unilateral ureteral obstruction” by Mizuguchi, Y., Chen, J., Seshan, S. V., Poppas, D. P., Szeto, H. H., & Felsen, D., published in the American Journal of Physiology – Renal Physiology in 2008, investigates the effects of a new antioxidant peptide in reducing kidney damage and cell death in cases of unilateral ureteral obstruction. This study contributes to understanding potential treatments for kidney injuries caused by obstructive conditions, focusing on the role of this specific peptide in protecting renal tissue.
Read the full article https://journals.physiology.org/doi/abs/10.1152/ajprenal.00395.2007
Saad, A., Herrmann, S., Eirin, A., Ferguson, C. M., Glockner, J. F., Bjarnason, H., McKusick, M. A., Misra, S., Lerman, L. O., & Textor, S. C. (2017). Phase 2a Clinical Trial of Mitochondrial Protection (Elamipretide) During Stent Revascularization in Patients With Atherosclerotic Renal Artery Stenosis. Circulation. Cardiovascular interventions, 10(9), e005487. https://doi.org/10.1161/CIRCINTERVENTIONS.117.005487
Phase 2a Clinical Trial of Mitochondrial Protection (Elamipretide) During Stent Revascularization in Patients With Atherosclerotic Renal Artery Stenosis
The article titled “Phase 2a Clinical Trial of Mitochondrial Protection (Elamipretide) During Stent Revascularization in Patients With Atherosclerotic Renal Artery Stenosis” by Saad, A., Herrmann, S., Eirin, A., et al., published in “Circulation. Cardiovascular Interventions” in 2017, explores the effects of elamipretide, a mitochondrial-targeted peptide, in the context of stent revascularization in patients with atherosclerotic renal artery stenosis. This clinical trial aims to assess the efficacy of elamipretide in protecting renal function during revascularization procedures.
Read the full article https://www.ahajournals.org/doi/abs/10.1161/CIRCINTERVENTIONS.117.005487
Miyamoto, S., Zhang, G., Hall, D., Oates, P. J., Maity, S., Madesh, M., Han, X., & Sharma, K. (2020). Restoring mitochondrial superoxide levels with elamipretide (MTP-131) protects db/db mice against progression of diabetic kidney disease. The Journal of biological chemistry, 295(21), 7249–7260. https://doi.org/10.1074/jbc.RA119.011110
Restoring mitochondrial superoxide levels with elamipretide (MTP-131) protects db/db mice against progression of diabetic kidney disease
The article titled “Restoring mitochondrial superoxide levels with elamipretide (MTP-131) protects db/db mice against progression of diabetic kidney disease,” authored by Miyamoto, S., Zhang, G., Hall, D., et al., and published in The Journal of Biological Chemistry in 2020, examines the protective effects of elamipretide on diabetic kidney disease. This study focuses on the role of elamipretide in managing mitochondrial superoxide levels and its potential in mitigating the progression of kidney disease in diabetic mice models.
Read the full article https://www.jbc.org/article/S0021-9258(17)50260-4/abstract
Zhu, Y., Luo, M., Bai, X., Li, J., Nie, P., Li, B., & Luo, P. (2022). SS-31, a Mitochondria-Targeting Peptide, Ameliorates Kidney Disease. Oxidative medicine and cellular longevity, 2022, 1295509. https://doi.org/10.1155/2022/1295509.
SS-31, a mitochondria-targeting peptide, ameliorates kidney disease
The 2022 article “SS-31, a Mitochondria-Targeting Peptide, Ameliorates Kidney Disease” by Zhu, Y., Luo, M., Bai, X., et al., published in “Oxidative Medicine and Cellular Longevity,” investigates the therapeutic effects of SS-31 on kidney disease. This study specifically explores how SS-31, by targeting mitochondrial dysfunction, could positively impact kidney health and potentially offer a new avenue for treating kidney-related disorders.
Read the full article https://www.hindawi.com/journals/omcl/2022/1295509/
Daneshgar, N., Liang, P. I., Lan, R. S., Horstmann, M. M., Pack, L., Bhardwaj, G., Penniman, C. M., O’Neill, B. T., & Dai, D. F. (2022). Elamipretide treatment during pregnancy ameliorates the progression of polycystic kidney disease in maternal and neonatal mice with PKD1 mutations. Kidney international, 101(5), 906–911. https://doi.org/10.1016/j.kint.2021.12.006
Elamipretide treatment during pregnancy ameliorates the progression of polycystic kidney disease in maternal and neonatal mice with PKD1 mutations
The 2022 study “Elamipretide treatment during pregnancy ameliorates the progression of polycystic kidney disease in maternal and neonatal mice with PKD1 mutations,” by Daneshgar, N., Liang, P. I., Lan, R. S., et al., published in “Kidney International,” focuses on the effects of elamipretide treatment on polycystic kidney disease (PKD) in pregnant mice and their offspring. This research investigates how elamipretide, known for targeting mitochondrial function, might influence the progression of PKD, particularly in the context of maternal and neonatal health.
Read the full article https://www.sciencedirect.com/science/article/pii/S0085253821011649
Szeto HH, Liu S, Soong Y, Seshan SV, Cohen-Gould L, Manichev V, Feldman LC, Gustafsson T. Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1β and IL-18 and Arrests CKD. J Am Soc Nephrol. 2017 May;28(5):1437-1449. doi: 10.1681/ASN.2016070761. Epub 2016 Nov 23. PMID: 27881606; PMCID: PMC5407729.
Mitochondria protection after acute ischemia prevents prolonged upregulation of IL-1β and IL-18 and arrests CKD
The 2017 study “Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1β and IL-18 and Arrests CKD” by Szeto HH, Liu S, Soong Y, et al., published in the Journal of the American Society of Nephrology, investigates the effects of mitochondrial protection on chronic kidney disease (CKD) progression following acute ischemia. The study focuses on how safeguarding mitochondria can mitigate inflammation and halt the advancement of CKD, providing insights into potential therapeutic strategies for kidney diseases.
Read the full article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5407729/
Szeto H. H. (2017). Pharmacologic Approaches to Improve Mitochondrial Function in AKI and CKD. Journal of the American Society of Nephrology : JASN, 28(10), 2856–2865. https://doi.org/10.1681/ASN.2017030247.
Pharmacologic Approaches to Improve Mitochondrial Function in AKI and CKD
The 2017 article “Pharmacologic Approaches to Improve Mitochondrial Function in AKI and CKD” by Szeto H. H., published in the Journal of the American Society of Nephrology, discusses strategies for enhancing mitochondrial function as a therapeutic approach in acute kidney injury (AKI) and chronic kidney disease (CKD). The focus is on pharmacological interventions and their potential in mitigating the progression of these renal conditions by targeting mitochondrial pathways. This work emphasizes the importance of mitochondria in kidney health and disease.
Read the full article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5619975/
Sweetwyne, M. T., Pippin, J. W., Eng, D. G., Hudkins, K. L., Chiao, Y. A., Campbell, M. D., Marcinek, D. J., Alpers, C. E., Szeto, H. H., Rabinovitch, P. S., & Shankland, S. J. (2017). The mitochondrial-targeted peptide, SS-31, improves glomerular architecture in mice of advanced age. Kidney international, 91(5), 1126–1145. https://doi.org/10.1016/j.kint.2016.10.036.
The mitochondrial-targeted peptide, SS-31, improves glomerular architecture in mice of advanced age
The 2017 study “The mitochondrial-targeted peptide, SS-31, improves glomerular architecture in mice of advanced age” by Sweetwyne, M. T., Pippin, J. W., Eng, D. G., et al., published in Kidney International, examines the effects of SS-31 on kidney structure in aged mice. This research focuses on how the peptide SS-31, targeted at mitochondria, can positively impact the health of glomeruli, the filtering units in kidneys, particularly in the context of aging.
Read the full article https://www.sciencedirect.com/science/article/pii/S0085253816306524
Wyss, J. C., Kumar, R., Mikulic, J., Schneider, M., Mary, J. L., Aebi, J. D., Juillerat-Jeanneret, L., & Golshayan, D. (2019). Differential Effects of the Mitochondria-Active Tetrapeptide SS-31 (D-Arg-dimethylTyr-Lys-Phe-NH2) and Its Peptidase-Targeted Prodrugs in Experimental Acute Kidney Injury. Frontiers in pharmacology, 10, 1209. https://doi.org/10.3389/fphar.2019.01209.
Differential Effects of the Mitochondria-Active Tetrapeptide SS-31 (D-Arg-dimethylTyr-Lys-Phe-NH2) and Its Peptidase-Targeted Prodrugs in Experimental Acute Kidney Injury
The 2019 study “Differential Effects of the Mitochondria-Active Tetrapeptide SS-31 (D-Arg-dimethylTyr-Lys-Phe-NH2) and Its Peptidase-Targeted Prodrugs in Experimental Acute Kidney Injury” by Wyss, J. C., Kumar, R., Mikulic, J., et al., published in Frontiers in Pharmacology, examines the impacts of SS-31 and its prodrugs on acute kidney injury. This research explores how these compounds, with a focus on mitochondrial targeting, affect kidney health in an experimental setting, providing insights into potential therapeutic applications for kidney injuries.
Read the full article https://www.frontiersin.org/articles/10.3389/fphar.2019.01209/full
Kim SR, Eirin A, Zhang X, Lerman A, Lerman LO. Mitochondrial Protection Partly Mitigates Kidney Cellular Senescence in Swine Atherosclerotic Renal Artery Stenosis. Cell Physiol Biochem. 2019;52(3):617-632. doi: 10.33594/000000044. PMID: 30907989; PMCID: PMC6519989
Mitochondrial Protection Partly Mitigates Kidney Cellular Senescence in Swine Atherosclerotic Renal Artery Stenosis
The 2019 study “Mitochondrial Protection Partly Mitigates Kidney Cellular Senescence in Swine Atherosclerotic Renal Artery Stenosis” by Kim SR, Eirin A, Zhang X, et al., published in Cell Physiology and Biochemistry, explores the impact of mitochondrial protection on kidney cell aging in the context of atherosclerotic renal artery stenosis in swine. This research provides insights into how targeting mitochondria might alleviate cellular senescence in kidney diseases related to arterial stenosis.
Read the full article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6519989/
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