Figure 3: Effects of CD36 in diabetes cardiomyopathy.
In diabetes, increased insulin activates the PI3K-Akt pathway, thereby promoting the transportation of CD36 from the endosome to the cell membrane. FOXO transcription factor promotes the expression of CD36. Down-regulated mir-200b-3p and up-regulated mir-320 also accelerate the transcription and translation of CD36, thus further increasing the distribution of CD36 on the cell membrane, which facilitates the uptake of LCFA of the cardiomyocytes. LCFA promotes the transfer of CD36 in the endosome to the cell membrane, further increasing the distribution of CD36 on the cell membrane. Intracellular LCFA either enters the mitochondria for aerobic oxidation producing energy and the byproducts-ROS or forms triglyceride for energy storage, and the accumulation of triglyceride would trigger insulin resistance. Insulin resistance and ROS assembling deteriorate cardiac function and result in diabetic cardiomyopathy.