Abstract
Cluster of differentiation 36 (CD36), also referred to as scavenger receptor B2, has been shown to serve multiple functions in lipid metabolism, inflammatory signaling, oxidative stress, and energy reprogramming. As a scavenger receptor, CD36 interacts with various ligands, such as oxidized low-density lipoprotein (oxLDL), thrombospondin 1 (TSP-1), and fatty acid (FA), thereby activating specific downstream signaling pathways. Cardiac CD36 is mostly expressed on the surface of cardiomyocytes and endothelial cells. The pathophysiological process of diabetic cardiomyopathy (DCM) encompasses diverse metabolic abnormalities, such as enhanced transfer of cardiac myocyte sarcolemmal FA, increased levels of advanced glycation end-products, elevation in oxidative stress, impaired insulin signaling cascade, disturbance in calcium handling, and microvascular rarefaction which are closely related to CD36 signaling. This review presents a summary of the CD36 signaling pathway that acts mainly as a long-chain FA transporter in cardiac myocytes and functions as a receptor to bind to numerous ligands in endothelial cells. Finally, we summarize the recent basic research and clinical findings regarding CD36 signaling in DCM, suggesting a promising strategy to treat this condition.
Highlights
Cluster of differentiation 36 (CD36) was first reported as glycoprotein IV in 1977, detected as the fourth obvious band upon SDS-polyacrylamide protein gel electrophoresis of human platelet membranes [1]
CD36 can bind to diverse ligands to trigger different signaling pathways during disease progression
We first described the basic structure of the CD36 protein and the CD36 regulation at transcriptional, translational and post-translational level
Summary
Cluster of differentiation 36 (CD36) was first reported as glycoprotein IV in 1977, detected as the fourth obvious band upon SDS-polyacrylamide protein gel electrophoresis of human platelet membranes [1]. It was subsequently demonstrated to be a macrophage receptor that mediated the uptake of oxidized LDL (oxLDL) and is involved in the phagocytosis of cells It is called as the scavenger receptor [2]. CD36deficient patients presented a dramatic reduction in myocardial uptake of long-chain fatty acids (LCFAs), whereas 18F-fluorodeoxyglucose (FDG) was increased in the myocardium [15, 16]. These metabolic changes were in accordance with the changes observed in CD36 knockout mice [17]. We found that nuclear miR-320 triggered the transcription of fatty acid metabolic genes, including CD36, to cause DCM [20]. We summarize the effects of CD36 in various pathophysiological processes and the current CD36related therapeutic strategies in DCM
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