Cellular oxidative stress response

The cellular oxidative stress response encompasses the suite of molecular and physiological adaptations cells activate to counter excess reactive oxygen species (ROS) and other oxidants. It involves activation of defenses like antioxidant enzymes (e.g., superoxide dismutase, catalase, glutathione peroxidase), signaling cascades (e.g., Nrf2 pathway), and changes in gene expression, metabolism, and cell fate decisions such as apoptosis or autophagy. This response is essential for maintaining cellular homeostasis, modulating inflammation, repairing damage, and surviving environmental and endogenous insults. Dysregulation is implicated in diverse diseases, including cancer, neurodegeneration, cardiovascular and metabolic disorders[1][2][3][4][5][6][7][8][9]. The term does not map to a single actionable therapeutic target but instead refers to a broader biological stress response involving many molecular actors. For structured drug target information, focus should shift to specific molecules like "Nuclear factor erythroid 2-related factor 2 (Nrf2)", "Superoxide dismutase", or "Glutathione peroxidase", all of which are concrete molecular targets within the oxidative stress response pathway[5][3][2].

Other names

oxidative stress responsecellular redox responseoxidative stress adaptationresponse to reactive oxygen species