KMV-mediated cardiomyocyte-to-endothelial cell signaling drives capillary rarefaction to promote heart failure following pressure overload.

ABSTRACT: Rationale: Pressure overload (PO)-induced heart failure (HF) is a global health burden with poor outcomes. Cardiomyocyte hypertrophy and capillary rarefaction are two features and drivers of PO-induced HF. Metabolism is altered in hypertrophic cardiomyocytes; however, the metabolites secreted by hypertrophic cardiomyocytes to paracrinally regulate capillary density remain to be identified. Methods: PO-induced HF was established by transverse aortic constriction in mice. Metabolite secretion was examined by nontargeted metabolomics and enzyme-linked immunosorbent assays. Gene expression was examined by RNA-sequencing and immunoblotting. Protein-promoter binding was examined by chromatin immunoprecipitation-PCR. Cardiomyocyte hypertrophy and cardiac capillary density were exami

SUBMITTER: Gao C 

PROVIDER: S-EPMC12036891 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature