TASK-1 and TASK-3 channels modulate pressure overload-induced cardiac remodeling and dysfunction.

ABSTRACT: Tandem pore domain acid-sensitive K⁺ (TASK) channels are present in cardiac tissue; however, their contribution to cardiac pathophysiology is not well understood. Here, we investigate the role of TASK-1 and TASK-3 in the pathogenesis of cardiac dysfunction using both human tissue and mouse models of genetic TASK channel loss of function. Compared with normal human cardiac tissue, TASK-1 gene expression is reduced in association with either cardiac hypertrophy alone or combined cardiac hypertrophy and heart failure. In a pressure overload cardiomyopathy model, TASK-1 global knockout (TASK-1 KO) mice have both reduced cardiac hypertrophy and preserved cardiac function compared with wild-type mice. In contrast to the TASK-1 KO mouse pressure overload response, TASK-3 global knockou

SUBMITTER: Duan W 

PROVIDER: S-EPMC7099448 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature