ArticleFrontiers in physiology2025
Mitochondria-derived peptide MOTS-c restores mitochondrial respiration in type 2 diabetic heart.
Article in Frontiers in physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Mitokines as bioenergetic stress signals in cardiovascular disease: mitochondrial communication, endocrine adaptation, and translational implications.Journal of bioenergetics and biomembranes · 2026Review
- Mitochondrial peptide MOTS-c suppresses systemic and cardiac inflammasome activation in a diabetic rat model.Experimental physiology · 2026Article
- Substrate-specific mitochondrial dysfunction and metabolomic profiles in type 2 diabetic rat hearts.Experimental physiology · 2026Article
- Mitochondrial respiration and hydrogen peroxide production rate in right atrial tissues from obese diabetic patients.Experimental physiology · 2026Article
- Exogenous MOTS-c mitigates myocardial ischemia-reperfusion injury: experimental and in silico evidence from rat heart models.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Effects of graviola oil extract on fattening performance and circadian rhythms of adipokine, cardiac and mitochondrial function markers in lambs.BMC veterinary research · 2026Article
- Distinct profiles of mitochondrial bioenergetics and redox balance in left atrial and ventricular myocardium in the healthy rat heart.Experimental physiology · 2026Article
- Advances in the application of nanoparticles for the diagnosis and treatment of diabetic cardiomyopathy.Frontiers in cell and developmental biology · 2026Review
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4 authors.
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Abstract
Introduction: Type 2 diabetes (T2D) is a global epidemic, and heart failure is the primary cause of premature death among T2D patients. Mitochondrial dysfunction has been linked to decreased contractile performance in diabetic heart, partly due to a disturbance in the mitochondrial capacity to supply adequate metabolic energy to contractile proteins. MOTS-c, a newly discovered mitochondrial-derived peptide, has shown promise as a therapeutic for restoring energy homeostasis and muscle function in metabolic diseases. However, whether MOTS-c therapy improves T2D heart function by increasing mitochondrial bioenergetic function remains unknown. Methods: Here we studied the mitochondrial bioenergetic function of heart tissues isolated from a rat model mimicking type 2 diabetes induced by a high-fat diet and low-dose streptozotocin. Treated diabetic group received MOTS-c (15 mg/kg) daily injection for 3 weeks. We employed high-resolution respirometric and fluorometric techniques to simultaneously assess mitochondrial ATP production and hydrolysis capacity, reactive oxygen species (ROS) production, and oxygen flux in cardiac tissue homogenates. Results: We found that untreated T2D rats had hyperglycemia, poor glucose control, and left ventricular hypertrophy relative to controls. T2D mitochondria showed decreased oxygen flux at the oxidative phosphorylation (OXP) while ROS production, ATP production and hydrolysis rates remained unchanged. Diabetic rats treated with MOTS-c showed decreased fasting glucose levels, improved glucose homeostasis, and decreased degree of cardiac hypertrophy. At the subcellular level, MOTS-c treated mitochondria showed increased OXPHOS respiration and ROS levels and decreased ATP hydrolysis rate during anoxic conditions. Discussion: These findings demonstrate beneficial effects of MOTS-c treatment on glucose homeostasis and suggest a useful therapeutic option for diabetic-related cardiomyopathy and mitochondrial dysfunction.
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