Abstract
Fatty acid translocase cluster of differentiation (CD36) is a multifunctional membrane protein that facilitates the uptake of long-chain fatty acids. Lipophagy is autophagic degradation of lipid droplets. Accumulating evidence suggests that CD36 is involved in the regulation of intracellular signal transduction that modulates fatty acid storage or usage. However, little is known about the relationship between CD36 and lipophagy. In this study, we found that increased CD36 expression was coupled with decreased autophagy in the livers of mice treated with a high-fat diet. Overexpressing CD36 in HepG2 and Huh7 cells inhibited autophagy, while knocking down CD36 expression induced autophagy due to the increased autophagosome formation in autophagic flux. Meanwhile, knockout of CD36 in mice increased autophagy, while the reconstruction of CD36 expression in CD36-knockout mice reduced autophagy. CD36 knockdown in HepG2 cells increased lipophagy and β-oxidation, which contributed to improving lipid accumulation. In addition, CD36 expression regulated autophagy through the AMPK pathway, with phosphorylation of ULK1/Beclin1 also involved in the process. These findings suggest that CD36 is a negative regulator of autophagy, and the induction of lipophagy by ameliorating CD36 expression can be a potential therapeutic strategy for the treatment of fatty liver diseases through attenuating lipid overaccumulation.
Highlights
Fatty acid translocase cluster of differentiation (CD36) is a multifunctional membrane protein that facilitates the uptake of long-chain fatty acids
Our results demonstrate that the hepatocyte cluster of differentiation 36 (CD36) has a negative role in the regulation of lipophagy through an adenosine monophosphate-activated protein kinase (AMPK)-dependent pathway
Hematoxylin and eosin staining and Oil Red O staining showed evident steatosis in the livers of mice fed the high-fat diet (HFD) compared with the normal chow diet (NCD) (Fig. 1A)
Summary
Fatty acid translocase cluster of differentiation (CD36) is a multifunctional membrane protein that facilitates the uptake of long-chain fatty acids. CD36 expression regulated autophagy through the AMPK pathway, with phosphorylation of ULK1/Beclin involved in the process These findings suggest that CD36 is a negative regulator of autophagy, and the induction of lipophagy by ameliorating CD36 expression can be a potential therapeutic strategy for the treatment of fatty liver diseases through attenuating lipid overaccumulation.—Li, Y., P. The cluster of differentiation 36 (CD36) belongs to the scavenger receptor family, known as fatty acid translocase, that facilitates the uptake of long-chain fatty acids (LCFAs) and is widely expressed on the surface of many cell types in vertebrates [4, 5]. CD36 recognizes different ligands and may promote different intracellular signaling pathways This multifunctional membrane glycoprotein has been studied extensively in relation to its role in the uptake of LCFAs, which are involved in NAFLD.
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