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. 2022 Nov 4;16:3829–3845. doi: 10.2147/DDDT.S386982

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© 2022 Feng et al.

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The mechanisms of CD36 in NAFLD. (A). Molecular mechanisms by which CD36 palmitoylation promotes FAO and NAFLD. (B). Molecular mechanisms by which CD36 palmitoylation promotes β-oxidation and inflammation. (C). Molecular mechanisms by which CD36 inhibits autophagy. (D). Molecular mechanisms by which CD36 promotes De novo lipogenesis.

Abbreviations: NAFLD, nonalcoholic fatty liver disease; CD36, differentiated cluster 36; LCFA, long chain fatty acid; ACSL, long-chain acyl-CoA synthetase; FAO, free fatty acid oxidation; TG, triglycerides; LKB1, live kinase B1; JNK, c-JUN N-terminal kinase; AMPK, AMP-activated protein kinase; Lyn, the kinase Lck/Yes-related novel protein tyrosine kinase; FA, Fatty acid; AhR, aryl hydrocarbon receptor; PXR, Pregnane X receptor; PPARγ: peroxisome proliferator-activated receptorγ; LXR, liver X receptor; PCSK9, proprotein convertase subtilisin/kexin type 9; mTOR, mechanistic target of rapamycin; UCK1, uridine-cytidine kinase 1; LDs, lipid droplets; ER, endoplasmic reticulum; SCAP, SREBP cleavage-activating protein; INSIG2, insulin-induced gene-2; SREBP1, sterol regulatory element-binding protein 1.