ArticleScientific reports2023
The role of MOTS-c-mediated antioxidant defense in aerobic exercise alleviating diabetic myocardial injury.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Substrate-specific mitochondrial dysfunction and metabolomic profiles in type 2 diabetic rat hearts.Experimental physiology · 2026Article
- Mitochondrial peptide MOTS-c suppresses systemic and cardiac inflammasome activation in a diabetic rat model.Experimental physiology · 2026Article
- Mitochondrial-derived peptide MOTS-c activates metabolic signaling but blunts reparative function in human mesenchymal stromal cells.Inflammation and regeneration · 2026Article
- MOTS-c is associated with oxidative stress and arterial stiffness in peritoneal dialysis patients: a pilot study.International urology and nephrology · 2026Article
- Mitochondrial respiration and hydrogen peroxide production rate in right atrial tissues from obese diabetic patients.Experimental physiology · 2026Article
- Reduced serum and skeletal muscle MOTS c levels in women with polycystic ovary syndrome are associated with mitochondrial dysfunction.Scientific reports · 2026Article
- MOTS‑c protects against placental injury via Nrf2 activation in hypoxia‑induced intrauterine growth restriction mice.International journal of molecular medicine · 2026Article
- Aerobic exercise and MOTS-c attenuate diabetic myocardial fibrosis via inhibition of the THBS1/TGF-β signaling pathway.Frontiers in endocrinology · 2026Article
- Simple molecules make difference: short peptides play a novel role in slowing senescence.npj aging · 2025Review
- AAV-mediated STC-1 expression mitigates neuroinflammation and preserves visual function in degenerative retinopathy.Journal of translational medicine · 2025Article
- Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes.Experimental & molecular medicine · 2025Article
- Characterization of the Avian Mitochondrial-Derived Peptide MOTS-c and Its Potential Role as a Metabolic Regulator.Animals : an open access journal from MDPI · 2025Article
- Reduced serum levels of mitochondria-derived peptide MOTS-c in patients with obstructive sleep apnea.Sleep and biological rhythms · 2025Article
- MOTS-c mimics exercise to combat diabetic liver fibrosis by targeting Keap1-Nrf2-Smad2/3.Scientific reports · 2025Article
- Non-canonical ORFs-derived protein products in mitochondria: A multifaceted exploration of their functions in health and disease.Protein science : a publication of the Protein Society · 2025Review
- Mitochondria-derived peptide MOTS-c restores mitochondrial respiration in type 2 diabetic heart.Frontiers in physiology · 2025Article
- MOTS-c as a Potential Diagnostic-prognostic Biomarker for Myocardial Infarction.Cardiovascular & hematological agents in medicinal chemistry · 2025Article
- Circulating PGC-1α and MOTS-c Peptide as Potential Mitochondrial Biomarkers in Patients Undergoing Aortic Valve Replacement.Biologics : targets & therapy · 2025Article
- Metabolomic Profiling Reveals That Exercise Lowers Biomarkers of Cardiac Dysfunction in Rats with Type 2 Diabetes.Antioxidants (Basel, Switzerland) · 2024Article
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Authors and funding
12 authors.
Funding
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Abstract
Myocardial remodeling and dysfunction are commonly observed in type 2 diabetes mellitus (T2DM). Aerobic exercise can partly alleviate diabetes-induced myocardial dysfunction through its antioxidant actions. MOTS-c is a potential exercise mimic. This study aimed to investigate the effects of MOTS-c on improving diabetic heart function and its mechanism and to identify whether MOTS-c improved antioxidant defenses due to aerobic exercise. Herein, we established a rat model of T2DM induced by high-fat diet combined with a low-dose streptozotocin injection. Interventions were performed using intraperitoneal injections of MOTS-c (i.p. 0.5 mg/kg/day, 7 days/week) or aerobic exercise training (treadmill, 20 m/min, 60 min/day, 5 days/week) for 8 weeks. Myocardial ultrastructure was assessed using transmission electron microscopy (TEM), myocardial lipid peroxidation levels (MDA), superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) levels were assessed using colorimetric methods, and molecular analyses including MOTS-c, Kelch-like ECH-associated protein 1 (Keap1), Nuclear factor E2-related factor 2 (Nrf2), adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)and phospho-AMPK (p-AMPK) were examined using Western blot. The results showed that MOTS-c, with or without exercise, reduced myocardial ultrastructural damage and improved glucolipid metabolism and cardiac function in T2DM. Furthermore, MOTS-c increased antioxidant markers such as SOD, CAT, and the protein expression of myocardial MOTS-c, Keap1, Nrf2, and p-AMPK. MOTS-c with exercise treatment reduced myocardial MDA and increased p-AMPK significantly comparing to only exercise or MOTS-c alone. Our findings suggest that MOTS-c may be a helpful supplement for overcoming exercise insufficiency and improving myocardial structure and function in diabetes.
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