Study record
Exogenous MOTS-c mitigates myocardial ischemia-reperfusion injury: experimental and in silico evidence from rat heart models
Santhanam SS, Jayaraman S, Kurian GA · Naunyn Schmiedebergs Arch Pharmacol · 2026
What this study reported
Reported in isolated perfused rat hearts that MOTS-c added to the perfusion buffer at reperfusion was associated with smaller infarct size, improved heart rate, left ventricular developed pressure and rate-pressure product, lower end-diastolic pressure and less lactate dehydrogenase release than ischemia-reperfusion alone. Found higher superoxide dismutase, catalase and glutathione redox ratio with less lipid peroxidation, normalised myeloperoxidase activity, downregulated caspase 3, 7 and 9, BAX and PARP, and upregulated BCL2, GPX4 and FOXO in the same hearts. Reported computational docking predicting interactions of MOTS-c with MAPK, mTOR, AMPK, NRF2, PI3K and caspase 3.
Limitations
Isolated-heart preparation lacking systemic, neural and humoral influences, male rats only with group sizes not reported in the abstract, a narrow range of exposures tested, and mechanistic claims resting partly on in silico docking rather than measured binding.
Study record
| Study model | Tissue / sample study (ex vivo) |
|---|---|
| Substance studied | MOTS-c administeredSynthetic MOTS-c was given to cells, animals or people. |
| Species | rat |
| System studied | Isolated Langendorff-perfused male Sprague-Dawley rat hearts subjected to global ischemia and reperfusion; molecular docking |
| Population | Not reported |
| Design | Ex vivo isolated-heart experiment with in silico molecular docking |
| Sample size as reported | Not reported |
| Control group | hearts subjected to ischemia-reperfusion without MOTS-c |
| Route (data field only) | other |
| Endpoints measured | infarct size; hemodynamics (heart rate, left ventricular developed pressure, end-diastolic pressure); lactate dehydrogenase release; oxidative stress and antioxidant markers; apoptotic and cytoprotective gene expression; predicted peptide-protein interactions |
| Pathways measured | Oxidative stress · Apoptosis · Inflammation · AMPK signalling · NRF2 / antioxidant response · MAPK signalling |
| Research areas | Cardiovascular · Mitochondrial biology |
| Evidence tier | D — Cell, tissue or analytical |
| Publication types | Journal Article |
Appraisal
Each dimension is recorded separately and never combined into a single score. A study can be well controlled and still tell you little about people.
- Relevance to MOTS-c
- Direct
- Model applicability
- Mammalian
- Sample size
- Not reported
- Controls
- Appropriate
- Outcome validity
- Surrogate
- Support for its own conclusion
- Moderate
Provenance
- Bibliographic fields retrieved from PubMed E-utilities efetch (title, journal, date, authors, DOI) on 2026-11-11.
- Annotated from the published abstract.
- Editorial review: approved (2026-11-11).
- Classification follows the site methodology; the record describes the study, not what MOTS-c does in people.