Transcutaneous Electrical Acupoint Stimulation Ameliorates Cognitive Function through PINK1/Parkin Mediated Mitophagy in VD Rats

Figure 4

Molecular mechanism of PINK1/Parkin involved in mitophagy. After cerebral ischemia injury, AMPK inhibits mTOR and phosphorylates ULK1. Then, ULK1 recruited and activated the PI3K complex to generate PI3P. Meanwhile, PINK1 accumulates in the outer membrane of mitochondria and recruits Parkin. Parkin ubiquitinated proteins on the outer membrane of mitochondria are recognized by p62. p62 and LC3-II interact to form a complex that is encapsulated by autophagosomes. Autophagosomes fuse with lysosomes to form autophagolysosomes, which target mitochondria to complete clearance.