The Role of CD36 in Cardiovascular Disease: A Critical Review

CD36, also known as the scavenger receptor B2, is a multifunctional receptor widely expressed in various organs. CD36 is expressed in various tissues, including endothelial cells, cardiac muscle cells, renal tubular epithelial cells, liver cells, adipocytes, platelets, and macrophages, and is involved in many pathophysiological processes, including immune regulation and metabolic regulation. CD36 plays a crucial role in the uptake of long-chain fatty acids, the main metabolic substrate in myocardial tissue. The maturation and transportation of CD36 is regulated by post-translational modifications, including phosphorylation, ubiquitination, glycosylation, and palmitoylation. CD36 is decreased in pathological cardiac hypertrophy caused by ischaemia–reperfusion and pressure overload, and increased in diabetic cardiomyopathy and atherosclerosis. Deficiency of CD36 alleviates diabetic cardiomyopathy and atherosclerosis, while overexpression of CD36 eliminates ischaemia–reperfusion damage, together suggesting that CD36 is closely associated with the progression of cardiovascular diseases and may be a new therapeutic target. Transcriptional activation, post-translational modification, and localization changes of CD36 may provide new directions for the treatment of cardiovascular diseases. This review summarizes the regulation and post-translational modifications of CD36 and evaluates its role in cardiovascular diseases and its potential as a therapeutic target.