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Reactive oxygen species (ROS) and oxidative stress-related pathways represent a broad category of biochemical processes involving the generation and detoxification of reactive oxygen species, such as superoxide and hydrogen peroxide. These pathways are essential for normal physiological signaling, including the regulation of vascular tone and immune response, but their dysregulation leads to oxidative stress and macromolecular damage (Pizzino et al., 2017). In disease states like atherosclerosis, Parkinson's disease, and various cancers, chronic oxidative stress drives inflammation and cell death (Sies et al., 2017). Pharmacological intervention typically targets specific nodes within these pathways, such as the Nrf2/KEAP1 system to enhance endogenous antioxidant capacity or the inhibition of ROS-generating enzymes like NADPH oxidase (NOX) (He et al., 2020). Clinical candidates like bardoxolone methyl and established drugs like dimethyl fumarate modulate these pathways to treat inflammatory and autoimmune conditions (Liby & Sporn, 2012). However, the therapeutic window is narrow, as excessive antioxidant activity can interfere with essential redox-dependent signaling and host defense mechanisms (Gutteridge & Halliwell, 2018).
Direct scavenging of reactive oxygen species, induction of endogenous antioxidant enzymes via Nrf2 activation, and inhibition of ROS-producing enzymes such as NADPH oxidase (NOX) or xanthine oxidase.
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