Study type: In vitro · Status: Verified against declared source

MOTS-c attenuates lung ischemia-reperfusion injury via MYH9-Dependent nuclear translocation and transcriptional activation of antioxidant genes.

Redox biology · 2025

Study scale: The mitochondrial origin and clear biological role of MOTS-c make it a potential disease biomarker.

Product or molecular entity relationships

MOTS-c: Exact entity relationship. Legacy citation custody associates this source with the catalog record; no product-relevance conclusion is implied.

Plain-language verified summary

Question

Central to this study is the discovery that MOTS-c nuclear translocation is mechanistically coupled to oxidative stress via MYH9 phosphorylation.

Methods

Cardiopulmonary bypass (CPB) induces profound hemodynamic and physiologic perturbations, predisposing patients to various complications.

Scale or participants

The mitochondrial origin and clear biological role of MOTS-c make it a potential disease biomarker.

Key findings

Acute respiratory distress syndrome (ARDS) following cardiopulmonary bypass (CPB) is driven by oxidative stress during lung ischemia-reperfusion injury (LIRI).

Limitations and uncertainty

Cardiopulmonary bypass (CPB) induces profound hemodynamic and physiologic perturbations, predisposing patients to various complications.

Verified against declared source. Verification is limited to the declared source and review scope. It does not mean independent replication or establish efficacy, safety, or suitability.