Downregulation of TCF19 and ATAD2 causes endothelial cell cycle arrest at the transition from cardiac hypertrophy to heart failure.

ABSTRACT: Cardiac hypertrophy is a key mechanism that allows the heart to adapt to increased load, but in the long term is associated with a higher risk for heart failure, arrhythmia, and death. During hypertrophic growth, cardiac myocytes signal to endothelial cells via vascular endothelial growth factor (VEGF) to promote angiogenesis and maintain myocardial oxygen supply. Insufficient angiogenesis leads to a decline in capillary density and drives the progression from compensated cardiac hypertrophy to heart failure. Here, we studied the time course of endothelial cell gene expression during heart failure development and identified transcriptional regulators of cell proliferation and angiogenesis. We applied transverse aortic constriction (TAC) in mice and isolated cardiac endothelial cells for RN

SUBMITTER: Erny E 

PROVIDER: S-EPMC12680863 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature