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.