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. Author manuscript; available in PMC: 2020 Jun 1.
Published in final edited form as: Best Pract Res Clin Haematol. 2019 May 24;32(2):145–153. doi: 10.1016/j.beha.2019.05.008

Figure 1.

Figure 1.

Mitochondrial pathways of apoptosis and venetoclax mechanism of action. In response to cellular stress, the pro-apoptotic proteins BAX and BAK are translocated to the mitochondria and induce the permeabilization of the outer mitochondrial membrane with release of cytochrome c (Cyt C) into the cytoplasm. The Cyt C/Apaf-1 complex activates caspase 9 and the caspase cascade, inducing apoptosis. The mitochondrial pathway is regulated by pro-apoptotic BH3-only proteins, which activate BAX and inhibit BCL-2 and MCL-1. BCL-2, MCL-1 and BCL-X regulate cell survival by inactivation of the pro-apoptotic proteins. Venetoclax triggers apoptosis by selective inhibition of BCL-2, leading to the release of Cyt C and cell death.