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.