The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review

Figure 1

Process and regulatory mechanism of autophagy. MTOR inhibits the initiation of autophagy by inhibiting the Atg1 (mammalian ULK1). Various substances and stimuli can induce autophagy through the mTOR pathway, such as amino acids, energy, and oxidative stress. In chondrocytes, when mTOR is activated, it inhibits the expression of ULK1 and then affects the formation of ULK1, FIP200, and Atg13 complexes to inhibit the assembly of autophagic bodies. The function of beclin-1 in autophagy is regulated by Bcl-2, and Bcl-2 inhibits autophagy by combining and isolating beclin-1 under nutrient rich conditions. The induction of autophagy requires the dissociation of beclin-1 from Bcl-2. The formation of phagophore is driven by the beclin-1 associated class III PI3 Kinase with phosphatidylinositol3-phosphate-containing vesicles. The phagophore undergoes elongation and completion driven by two ubiquitin-related conjugation systems, the LC3-PE and Atg12-Atg5. Then, the autophagosome is fused with the lysosome. Finally, the substance degrades in the autolysosome and provides nutrients for the cells.