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. Author manuscript; available in PMC: 2022 Oct 1.
Published in final edited form as: Trends Cell Biol. 2022 Apr 25;32(10):841–853. doi: 10.1016/j.tcb.2022.03.012

Fig.5. Apoptosis.

Fig.5.

Proximal tubule apoptosis is a prominent feature of acute and chronic kidney disease. Intrinsic apoptosis is triggered by mitochondria damage. BCL2-associated X protein (BAX)/ BCL2-antagonist/killer (BAK) pores in the outer membrane of mitochondria will cause translocation of cytochrome c from the mitochondria to the cytosol to initiate the formation of the apoptosome consisting of caspase-9, Apaf1, and cytochrome-c. The apoptosome will activate executionary caspases such as caspase-3. Apoptosis will cause epithelial cell loss. Animal studies, analyzing BAX/BAK double KO, Caspase-9, and Caspase-3 KO mice or chemical caspase-inhibitors indicated the protective role of apoptosis from kidney disease development.