Study record
The mitochondrial-derived peptide MOTS-c suppresses ferroptosis and alleviates acute lung injury induced by myocardial ischemia reperfusion via PPARγ signaling pathway
Lu P, Li X, Li B et al. · Eur J Pharmacol · 2023
What this study reported
Measured circulating MOTS-c and malondialdehyde by ELISA in patients after off-pump coronary artery bypass grafting and found lower circulating MOTS-c in those with postoperative acute lung injury. In rats with myocardial ischaemia-reperfusion, reported that MOTS-c pretreatment reduced ferroptosis markers and lung histological injury in a manner dependent on PPARgamma signalling, and in MLE-12 cells reported that MOTS-c inhibited hypoxia-reoxygenation-induced ferroptosis through PPARgamma.
Limitations
Sample sizes not reported for the patient or animal groups; the human component is an uncontrolled observational measurement; animal and cell findings rest on a single rat model and a single mouse cell line, and PPARgamma dependence is inferred without reported genetic knockdown detail in the abstract.
Study record
| Study model | Human observational |
|---|---|
| Substance studied | SeveralMore than one of these is central to the paper (common for reviews). |
| Species | human, rat, mouse |
| System studied | Patients undergoing off-pump coronary artery bypass grafting; Sprague-Dawley rats with myocardial ischaemia-reperfusion; MLE-12 mouse lung epithelial cells under hypoxia-reoxygenation |
| Population | Patients undergoing off-pump coronary artery bypass grafting, with and without postoperative acute lung injury |
| Design | Clinical biomarker measurement with controlled animal and cell-culture experiments |
| Sample size as reported | not reported |
| Control group | patients without postoperative acute lung injury; untreated ischaemia-reperfusion rats; Ferrostatin-1 and Fe-citrate(III) comparator groups; untreated hypoxia-reoxygenation cells |
| Route (data field only) | other |
| Endpoints measured | circulating MOTS-c levels; malondialdehyde levels; lung histology; ferroptosis-related gene expression; PPARgamma protein expression |
| Pathways measured | Oxidative stress · Lipid metabolism · Other |
| Research areas | Lung · Cardiovascular |
| Evidence tier | B — Other human study |
| 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
- Human
- Sample size
- Not reported
- Controls
- Limited
- 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.