Progress in the application of mesenchymal stem cells to attenuate apoptosis in diabetic kidney disease

Figure 1 Pathways of apoptosis. A: Mitochondrial pathway: When the inside of the cell is stimulated, pro-apoptotic proteins such as Bax and Bak are activated and inserted into the mitochondrial membrane, increasing the permeability of the mitochondrial membrane and releasing cytochrome C into the cytoplasm. Cytochrome C combines with Apaf-1 to form an apoptosome, which recruits and activates Caspase-9, and then activates downstream effector caspases, leading to apoptosis; B: Death receptor pathway: Apoptotic signaling molecules outside the cell, such as tumor necrosis factor-α and FasL, bind to the death receptors on the cell surface to form a death-inducing signaling complex. After Caspase-8 is activated, it directly activates downstream effector caspases to trigger apoptosis. It can also activate the endogenous mitochondrial pathway by cleaving the Bid protein to amplify the apoptotic signal; C: Endoplasmic reticulum pathway: When the endoplasmic reticulum undergoes stress due to the accumulation of misfolded proteins, etc., it initiates the unfolded protein response. Through pathways such as the PERK-eIF2α-ATF4 pathway and the IRE1α pathway, it induces the expression of pro-apoptotic genes. At the same time, the endoplasmic reticulum releases calcium ions into the cytoplasm and activates relevant enzymes, such as Caspase-12, etc., ultimately inducing apoptosis. TNF: Tumor necrosis factor. It was drawn using Figdraw software.