ArticleJournal of physiology and biochemistry2018
Protective effects of mitochondrion-targeted peptide SS-31 against hind limb ischemia-reperfusion injury.
Article in Journal of physiology and biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 54 citations in OpenAlex.
- The Effects of Iloprost on Isthmin-1, Adropin and Trpc6 Immunoreactivity in an Experimental Lower Extremity Ischemia-Reperfusion Injury Model.Biomedicines · 2026Article
- Advances in the treatment of lower-extremity ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- SS-31: A promising therapeutic agent against bleomycin-induced pulmonary fibrosis in Mice.PloS one · 2025Article
- Identification and validation of mitochondrial-related genes in intestinal ischemia-reperfusion injury based on WGCNA and machine learning.Frontiers in molecular biosciences · 2025Article
- Mitochondrial destabilization in tendinopathy and potential therapeutic strategies.Journal of orthopaedic translation · 2024Review
- Article
- Mitochondrial antioxidant elamipretide improves learning and memory impairment induced by chronic sleep deprivation in mice.Brain and behavior · 2024Article
- Real-time imaging of mitochondrial redox reveals increased mitochondrial oxidative stress associated with amyloid β aggregates in vivo in a mouse model of Alzheimer's disease.Molecular neurodegeneration · 2024Article
- Elamipretide reduces pyroptosis and improves functional recovery after spinal cord injury.CNS neuroscience & therapeutics · 2023Article
- Hormone replacement therapy for postmenopausal atherosclerosis is offset by late age iron deposition.eLife · 2023Article
- Elamipretide alleviates pyroptosis in traumatically injured spinal cord by inhibiting cPLA2-induced lysosomal membrane permeabilization.Journal of neuroinflammation · 2023Article
- Mitochondrial Dysfunction in Cardiovascular Diseases: Potential Targets for Treatment.Frontiers in cell and developmental biology · 2022Review
- SS-31 Protects Liver from Ischemia-Reperfusion Injury via Modulating Macrophage Polarization.Oxidative medicine and cellular longevity · 2021Article
- Mitochondrial-Targeting Antioxidant SS-31 Suppresses Airway Inflammation and Oxidative Stress Induced by Cigarette Smoke.Oxidative medicine and cellular longevity · 2021Article
- Natural Antioxidants Improve the Vulnerability of Cardiomyocytes and Vascular Endothelial Cells under Stress Conditions: A Focus on Mitochondrial Quality Control.Oxidative medicine and cellular longevity · 2021Review
- Article
- Regulation of Mitochondrial Quality Control by Natural Drugs in the Treatment of Cardiovascular Diseases: Potential and Advantages.Frontiers in cell and developmental biology · 2020Review
- Mitochondria-Targeted Antioxidants: A Step towards Disease Treatment.Oxidative medicine and cellular longevity · 2020Review
- Protective effects of SS-31 against SDHB suppression-mitochondrial dysfunction-EndMT axis-modulated CBT sclerosis and progression.American journal of translational research · 2020Article
- Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic and memory impairment induced by lipopolysaccharide in mice.Journal of neuroinflammation · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Hind limb ischemia-reperfusion injury is an important pathology in vascular surgery. Reactive oxygen species are thought to be involved in the pathogenesis of hind limb ischemia-reperfusion injury. SS-31, which belongs to a family of mitochondrion-targeted peptide antioxidants, was shown to reduce mitochondrial reactive oxygen species production. In this study, we investigated whether the treatment of SS-31 could protect hind limb from ischemia-reperfusion injury in a mouse model. The results showed that SS-31 treatment either before or after ischemia exhibited similar protective effects. Histopathologically, SS-31 treatment prevented the IR-induced histological deterioration compared with the corresponding vehicle control. SS-31 treatment diminished oxidative stress revealed by the reduced malondialdehyde level and increased activities and protein levels of Sod and catalase. Cellular ATP contents and mitochondrial membrane potential increased and the level of cytosolic cytC was decreased after SS-31 treatment in this IR model, demonstrating that mitochondria were protected. The IR-induced increase of levels of inflammatory factors, such as Tnf-α and Il-1β, was prevented by SS-31 treatment. In agreement with the reduced cytosolic cytC, cleaved-caspase 3 was kept at a very low level after SS-31 treatment. Overall, the effect of SS-31 treatment before ischemia is mildly more effective than that after ischemia. In conclusion, our results demonstrate that SS-31 confers a protective effect in the mouse model of hind limb ischemia-reperfusion injury preventatively and therapeutically.
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