Apoptosis pathway via reactive oxygen species induction

The "Apoptosis pathway via reactive oxygen species induction" is not a single molecular target but rather describes a collection of cellular signaling events where increased levels of reactive oxygen species (ROS) trigger programmed cell death. This process involves both the intrinsic (mitochondrial) and extrinsic (death receptor-mediated) apoptotic pathways. In the intrinsic route, excessive ROS disrupt mitochondrial membranes through modulation by Bcl‑2 family proteins, leading to cytochrome c release and activation of caspases that execute apoptosis[1][2][4]. The extrinsic route can involve death receptors such as Fas or TNFR1 on the cell surface generating additional ROS upon ligand binding, further amplifying apoptotic signals[2][5]. Key regulatory nodes include p53 activation by DNA damage from oxidative stress and JNK signaling. While this mechanism is exploited therapeutically—particularly in cancer treatment where tumor cells are more susceptible to oxidative insults—it is not itself a discrete druggable protein or receptor but rather an entire network/process. Therefore, it should not be considered a canonical therapeutic target molecule but instead represents an important biological process relevant for drug action and toxicity assessment[1][5].

Other names

ROS-induced apoptosis pathwayReactive oxygen species-mediated apoptosisROS-dependent cell death pathway

Induction of oxidative stress leading to mitochondrial outer membrane permeabilization and cytochrome c release[1][2][4][5] Activation of pro-apoptotic signaling proteins such as p53 and JNK[1][3] Modulation of Bcl‑2 family proteins affecting mitochondrial integrity[4]