Oxidative stress and apoptotic pathways

Oxidative stress and apoptotic pathways refer to the interconnected biological processes where an imbalance between reactive oxygen species (ROS) production and antioxidant defenses leads to programmed cell death (Redza-Dutordoir & Averill-Bates, 2016, Biochimica et Biophysica Acta). Oxidative stress occurs when excessive free radicals cause damage to cellular lipids, proteins, and DNA, which subsequently triggers the apoptotic machinery, primarily through the mitochondrial (intrinsic) pathway (Sinha et al., 2013, Food and Chemical Toxicology). This process involves the release of cytochrome c and the activation of the caspase cascade, leading to systematic cell dismantling. These pathways are central to the pathogenesis of numerous conditions, including neurodegenerative diseases like Alzheimer's and Parkinson's, where chronic oxidative damage results in neuronal loss, and cancer, where ROS can both drive oncogenic mutations and be exploited to induce therapy-mediated cell death (Pizzino et al., 2017, Oxidative Medicine and Cellular Longevity). Because these pathways encompass a vast network of enzymes and signaling molecules rather than a single protein, they are classified as biological mechanisms or systems rather than discrete therapeutic targets. Consequently, drug development typically focuses on specific molecular components within these pathways, such as Nrf2 activators or Bcl-2 inhibitors, to achieve therapeutic modulation.

Other names

Oxidative stress-induced apoptosisROS-mediated cell deathRedox-regulated apoptotic signaling

Modulation of cellular redox balance and regulation of pro- and anti-apoptotic signaling molecules within the cell.