| Li 2027 Bioact Mater MOTS-c analogue or derivative | Animal MOTS-c conjugated to a self-assembling Q11 peptide as a hydrogel carrier for isolated mitochondria; rat myocardial infarction model and macrophages | Reported that a MOTS-c-Q11 peptide hydrogel extended the survival and enzyme activity of isolated mitochondria and increased their internalisation by macrophages through an AMPK-dependent mechanism. Reported that in a rat myocardial infarction model the combined system was associated with less M1 macrophage infiltration, less cardiomyocyte damage and improved cardiac function and remodelling. | MOTS-c is used as part of a conjugated biomaterial rather than as the free peptide, so its independent contribution is hard to isolate; group sizes not reported in the abstract; a single rat infarction model with short follow-up. | Evidence tier C |
| Musolino 2026 Int Urol Nephrol Endogenous MOTS-c measured | Human obs. Stable peritoneal dialysis patients; MOTS-c measured in serum, urine and peritoneal dialysate | Measured MOTS-c in serum, urine and dialysate of peritoneal dialysis patients and reported that higher urinary MOTS-c was associated with lower advanced oxidation protein products and with higher pulse wave velocity and left ventricular systolic function. Reported that higher dialysate MOTS-c was associated with lower pulse wave velocity and lower blood pressure. | Small single-centre pilot with no control group and cross-sectional correlations only; multiple comparisons across three compartments without adjustment. | Evidence tier B |
| Zhang 2026 Antioxidants (Basel) Endogenous MOTS-c measured | Human obs. Healthy young males stratified as elite track and field athletes, recreationally active and sedentary; serum MOTS-c and fitness testing | Measured progressively higher serum MOTS-c from sedentary to recreationally active to elite athlete groups of young males. Reported strong positive correlations of serum MOTS-c with peak oxygen uptake, superoxide dismutase, back muscle endurance and post-fatigue force, a strong inverse correlation with post-exercise malondialdehyde, and no significant correlation with handgrip strength. | Very small groups of 10 young males each; cross-sectional design precludes causal inference; multiple strong correlations in a small sample risk overfitting. | Evidence tier B |
| Wang 2026 Biochem Pharmacol MOTS-c administered | Animal db/db mice with diabetic nephropathy and HK-2 human proximal tubular cells with LARS1 overexpression | Reported that administered MOTS-c was associated with preserved urinary albumin-to-creatinine ratio, less tubular injury, less lipid deposition and less macrophage accumulation in db/db mice. Reported lower p16, gammaH2AX and SA-beta-gal signal and lower LARS1 with increased LC3-mediated lipid droplet clearance, with LARS1 overexpression in HK-2 cells and an autophagy inhibitor in mice reversing these changes. | Group sizes and sex not reported in the abstract; a single genetic diabetes model and one human tubular cell line; mechanism relies on a non-selective autophagy inhibitor. | Evidence tier C |
| Tsui 2026 Reprod Fertil MOTS-c administered | Cells Aging-associated HGL5 human granulosa cells, ex vivo oocytes from young and aged mice, and public ovarian transcriptomic datasets | Reported that MOTS-c increased mitochondrial mass, ATP-linked and maximal respiration and spare respiratory capacity and reduced proton leak in aging-associated human granulosa cells without increasing reactive oxygen species. Reported that ex vivo MOTS-c exposure increased first polar body positivity and mitochondria-associated fluorescence and lowered oxidative-stress fluorescence in aged mouse oocytes, though outcomes stayed below young-reference levels. | A single immortalised granulosa cell line plus ex vivo mouse oocytes, with replicate numbers not reported in the abstract; fertilisation, embryo development and live birth were not assessed; transcriptomic component is a reanalysis of public datasets. | Evidence tier D |