Study record
MOTS-c attenuates lung ischemia-reperfusion injury via MYH9-Dependent nuclear translocation and transcriptional activation of antioxidant genes
Li X, Zhan F, Qiu G et al. · Redox Biol · 2025
What this study reported
Reported that the rise in serum MOTS-c within 24 hours after cardiopulmonary bypass discriminated patients who developed ARDS better than traditional biomarkers in multivariate models (AUC 0.885). Found in rats and in endothelial cells that reactive oxygen species-dependent CK2A-mediated MYH9 phosphorylation accompanied MOTS-c binding to MYH9-γ-actin complexes and nuclear transport, with MOTS-c occupancy at antioxidant response element-containing promoters, and that administered MOTS-c was associated with less lung injury, oxidative damage, inflammation and mortality in the rat model.
Limitations
Cohort size and composition are not reported in the abstract and the prediction model is not externally validated; animal work used a single rat injury model and male-predominant sampling, and no human exposure to MOTS-c was tested.
Study record
| Study model | Human observational |
|---|---|
| Substance studied | SeveralMore than one of these is central to the paper (common for reviews). |
| Species | human, rat |
| System studied | Serum from patients after cardiopulmonary bypass; rat lung ischemia-reperfusion model; endothelial cells under hypoxia-reoxygenation |
| Population | Patients undergoing cardiopulmonary bypass, followed for acute respiratory distress syndrome |
| Design | Observational biomarker cohort combined with controlled animal and cell mechanistic experiments |
| Sample size as reported | not reported |
| Control group | Patients who did not develop ARDS; untreated injury-model rats and cells |
| Route (data field only) | Not reported |
| Endpoints measured | serum MOTS-c change after surgery and ARDS prediction; MOTS-c nuclear translocation and MYH9 binding; MYH9 Ser1943 phosphorylation; antioxidant gene transcription (HMOX1, NQO1); lung injury, oxidative damage and inflammation; mortality in the rat model |
| Pathways measured | Nuclear translocation · NRF2 / antioxidant response · Oxidative stress · Inflammation |
| Research areas | Lung · Cardiovascular · Mitochondrial biology · Inflammation & immunity |
| Evidence tier | B — Other human study |
| Publication types | Journal Article, Research Support, Non-U.S. Gov't |
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
- 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.