CD36 knockdown attenuates pressure overload-induced cardiac injury by preventing lipotoxicity and improving myocardial energy metabolism.

ABSTRACT: Introduction: The heart predominantly derives its energy from fatty acid (FA) oxidation. However, the uncoupling of lipid uptake and FA oxidation can result in abnormal cardiac lipid accumulation and lipotoxicity, particularly in the context of heart failure. CD36 is a critical mediator of FA uptake in cardiac tissue. Studies have shown that genetic deletion of CD36 can prevent the onset of cardiac hypertrophy and dysfunction in murine models of obesity and diabetes. Nevertheless, the precise role of CD36 knockdown or knockout in the development and progression of cardiac dysfunction under conditions of pressure overload remains unclear. Objective: This study aims to investigate the feasibility of CD36 partially knockdown in the prevention of cardiac lipotoxicity and function

SUBMITTER: Geng J 

PROVIDER: S-EPMC11866539 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature