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Oxidative stress signaling describes the cellular sensing and response network to increased reactive oxygen species, coordinating antioxidant defense, repair, apoptosis, and cell fate decisions via interconnected pathways such as MAPK, NRF2–KEAP1, FoxO, and p53. Dysfunctional or excessive signaling contributes to disease progression in cancer, neurodegeneration, cardiovascular and metabolic disorders. It is not a direct molecular target but comprises actionable nodes for therapeutic intervention.
Drugs typically act by: Activating antioxidant pathways (NRF2 signaling); Modulating kinase pathways (MAPK signaling: inhibiting ERK, activating p38 or JNK); Scavenging or reducing ROS (antioxidants); Regulating mitochondrial ROS production.
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