Inhibiting CD36 palmitoylation improves cardiac function post-infarction by regulating lipid metabolic homeostasis and autophagy.

ABSTRACT: Alterations in myocardial energy substrate metabolism and mitochondrial injury following myocardial infarction (MI) lead to structural and functional abnormalities of the heart. The fatty acid translocase CD36 (CD36) plays a pivotal role in regulating lipid homeostasis and mitochondrial metabolism. Here, we demonstrate that inhibiting the palmitoylation of CD36 and the resulting alteration in its subcellular localization alleviates lipid metabolism disorders and mitochondrial dysfunction in cardiomyocytes of male mice post-MI. Mechanistically, the inhibition of CD36 palmitoylation enhances cardiac function through a dual mechanism: first, by alleviating fatty acid overload mediated by plasma membrane CD36, thereby restoring lipid metabolic balance; second, by augmenting the activity of the

SUBMITTER: Zhang Q 

PROVIDER: S-EPMC12271414 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature