TRIM47 promotes cardiac ischemia/reperfusion injury

ABSTRACT: This study shows that TRIM47 is upregulated in cardiomyocytes during cardiac I/R injury in an EGR1-dependent manner, correlating with injury severity. Cardiomyocyte-specific TRIM47 overexpression worsens, while TRIM47 knockout alleviates, I/R-induced cardiac injury and dysfunction. Mechanistically, TRIM47 promotes K63-linked ubiquitination of FOXO1 at lysine 210, inducing its nuclear translocation. Nuclear FOXO1 then inhibits HNF4A transcriptional activity, leading to mitochondrial dysfunction, fatty acid oxidation defects, and aggravated cardiac injury. Therapeutic knockdown of TRIM47 after I/R injury effectively prevents cardiac remodeling and dysfunction. The TRIM47/FOXO1/HNF4A axis represents a promising therapeutic target for cardiac I/R injury.

INSTRUMENT(S): Liquid Chromatography MS - positive - hilic, Liquid Chromatography MS - negative - hilic

PROVIDER: MTBLS14676 | MetaboLights | 2026-08-28

REPOSITORIES: MetaboLights