Fig. 1

Mechanism of apoptosis. (1) After Fas and FasL are combined in the death receptor pathway, they recruit molecules, such as FADD, and activate caspase cascade reactions, including activation of caspase 8, caspase 3 and caspase 7. Caspase 8 activation can be blocked by C-FLIP. Then, caspase 3 and caspase 7 continue to cleave cell substrates, such as ICAD, and trigger apoptosis. (2) Caspase 3 and caspase 7 in the death receptor pathway may activate caspase 6 to cleave Bid into tBid, which is transferred to the mitochondria and induces the release of cytochrome c (cytc), AIF, Smac/DIABLO, Omi/HtrA2, etc. Cytc activates caspase 9, APAF1, etc. to cause apoptosis, and the other three inhibit the XIAP survival protein to promote apoptosis. (3) AIF translocation from the mitochondria to the nucleus may interact with EndoG to trigger DNA degradation and apoptosis. P53 induces apoptosis by transactivating the expression of various proapoptotic proteins. (4) Lysosomal permeabilization induces apoptosis through the release of ctsB and ctsD to activate the mitochondrial pathway. (5) Dysfunction of the endoplasmic reticulum leads to UPR-induced apoptosis by activating caspase 12, 9 and 3