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In the case of intrinsic apoptosis, which is mainly associated with mitochondrial dysfunction or ER stress, ROS can activate the cell cycle regulators p53 and JNK, which induce pro-apoptotic Bcl-2 family proteins such as Bak and Baxantagonists to anti-apoptotic proteins Bcl-xL and Bcl-2 in the outer mitochondrial membrane (OMM)eventually causing mitochondrial outer membrane permeabilization and subsequent apoptosis [136, 137]