MOTS-c

§ Primary literature

1. 1.Gudiksen A (2026). MOTS-c improves intrinsic muscle mitochondrial bioenergetic health and efficiency in a PGC-1α/AMPK-dependent manner. Free Radical Biology and Medicine.Rodent studyIn mouse models, the mitochondrial-derived peptide MOTS-c was associated with improved intrinsic skeletal-muscle mitochondrial bioenergetic health and efficiency, alongside altered reactive-oxygen-species handling, in a manner reported to depend on PGC-1α and AMPK signaling.
2. 2.Li Z (2026). Aerobic exercise and MOTS-c attenuate diabetic myocardial fibrosis via inhibition of the THBS1/TGF-β signaling pathway. Frontiers in Endocrinology.Rodent studyIn a diabetic rat model, aerobic exercise and the mitochondrial-derived peptide MOTS-c, alone or combined, were associated with improved glucose and lipid profiles and reduced myocardial collagen deposition, which the authors link to suppression of the THBS1/TGF-β signaling pathway.
3. 3.Jamnick NA (2026). MOTS-c partially protects against skeletal muscle deterioration in C26 cachexia. Frontiers in Medicine.Rodent studyIn a mouse model of cancer cachexia, exogenous MOTS-c was associated with partial preservation of skeletal-muscle mass without preventing overall body-weight loss, alongside modulation of FOXO signaling and partial restoration of PGC-1α expression relative to cachectic controls.
4. 4.Zhou (2024). The correlation between mitochondrial derived peptide (MDP) and metabolic states: a systematic review and meta-analysis. Diabetology & Metabolic Syndrome.ReviewThis systematic review and meta-analysis pooled reported circulating MOTS-c concentrations across metabolic states, describing significantly reduced plasma MOTS-c in diabetes and obesity in the primary analysis, and positive correlation of circulating MOTS-c with total cholesterol and LDL-c in the analyzed studies.