Figure 2.

CD36 signaling pathway in cardiomyocytes. Under normal conditions (left), CD36 transfers LCFAs into cardiomyocytes, and LCFAs can promote CD36 transcription via PPARα binding to PPRE. Moreover, CD36 recycling occurs between endosomes and sarcolemma upon physiological stress, such as insulin stress and muscle contraction. During conditions of lipids oversupply (right), increased CD36 activity can enhance LCFA uptake to cause insulin resistance, endosome-sarcolemma recycling abnormalities and increased ROS production. LCFA, long-chain fatty acid; FABPpm, plasma membrane-localized fatty acid binding protein; FABPc, cytoplasmic FABP; TAG, triacylglycerol; DAG, diacylglycerol; Cer, ceramide; FAO, fatty acid oxidation; PPARα, peroxisome proliferator-activated receptor alpha; PPRE, PPAR response element; TSS, transcription start site; AMPK, adenosine 5’-monophosphate (AMP)-activated protein kinase; TBC1D1, Tre-2/BUB2/cdc1 domain family 1; Rabs, Rab GTPase-activating proteins; IRS1, insulin receptor substrate 1; PI3K, phosphatidylinositol 3-kinase; AKT, protein kinase B; AS160, Akt substrate 160; GLUT4, translocation of glucose transport 4; PKC, protein kinase C; V1, v-ATPase sub-complex V1; V0, v-ATPase sub-complex V0; VAMP, vesicle-associated membrane protein.