Cardiac immune cell infiltration associates with abnormal lipid metabolism.

ABSTRACT: CD36 mediates the uptake of long-chain fatty acids (FAs), a major energy substrate for the myocardium. Under excessive FA supply, CD36 can cause cardiac lipid accumulation and inflammation while its deletion reduces heart FA uptake and lipid content and increases glucose utilization. As a result, CD36 was proposed as a therapeutic target for obesity-associated heart disease. However, more recent reports have shown that CD36 deficiency suppresses myocardial flexibility in fuel preference between glucose and FAs, impairing tissue energy balance, while CD36 absence in tissue macrophages reduces efferocytosis and myocardial repair after injury. In line with the latter homeostatic functions, we had previously reported that CD36^-/- mice have chronic subclinical inflammation. Lipids ar

SUBMITTER: Cifarelli V 

PROVIDER: S-EPMC9428462 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature