Deletion of Endothelial TRPV4 Protects Heart From Pressure Overload-Induced Hypertrophy.

ABSTRACT:

Background

Left ventricular hypertrophy is a bipolar response, starting as an adaptive response to the hemodynamic challenge, but over time develops maladaptive pathology partly due to microvascular rarefaction and impaired coronary angiogenesis. Despite the profound influence on cardiac function, the mechanotransduction mechanisms that regulate coronary angiogenesis, leading to heart failure, are not well known.

Methods

We subjected endothelial-specific knockout mice of mechanically activated ion channel, TRPV4 (transient receptor potential cation channel subfamily V member 4; TRPV4^ECKO) to pressure overload via transverse aortic constriction and examined cardiac function, cardiomyocyte hypertrophy, cardiac fibrosis, and apoptosis. Further, we measured microvascu

SUBMITTER: Adapala RK 

PROVIDER: S-EPMC10705842 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature