Figure 2: Effects of CD36 in ischemic/reperfusion.
During the ischemic phase, the distribution of CD36 on the cell membrane decreases, leading to a decline of LCFA uptake and LCFA entering the mitochondria for aerobic oxidation, while GLUT4 increases on the cell membrane. Due to ischemia and hypoxia, the anaerobic glycolysis process is enhanced, and produces a large quantity of protons, thus resulting in a low cytoplasmic pH. Hydrion subsequently prevents the transport of CD36 from the endosome to the cell membrane, and further inhibits the distribution of CD36 on the cell membrane. The relatively increased pyruvate acid enters the mitochondria for aerobic oxidation to produce ATP. During this process, the decrease of CD36 prevents the accumulation of toxic lipid, and indirectly promotes the aerobic oxidation of glucose, which is beneficial to the survival of myocardial cells during the ischemic phase. During the reperfusion phase, the anaerobic glycolysis process of glucose decreased and the rate of proton production decreased. However, due to the low pH caused by a large number of protons accumulated in the ischemic phase, the membrane distribution of CD36 remains at a low level. At the same time, the rate of LCFA entering the mitochondria for aerobic oxidation is enhanced because of the triglyceride accumulate in ischemic phase, which is an essential supplementary for energy production. During this process, the low level of CD36 helps reduce the accumulation of toxic lipid, and the aerobic oxidation of LCFA provides most of the energy for the myocardium.