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Reactive oxygen species (ROS)–related pathways encompass the biochemical processes involved in the generation, signaling, and detoxification of oxygen-derived free radicals and non-radical oxidants (Pizzino et al., Oxid Med Cell Longev, 2017). These pathways include the enzymatic production of ROS by NADPH oxidases and the mitochondrial electron transport chain, balanced by antioxidant systems such as superoxide dismutase and the glutathione system (Sies et al., Nat Rev Mol Cell Biol, 2017). While physiological levels of ROS are essential for cell signaling and immune function, excessive ROS accumulation leads to oxidative stress and damage to cellular macromolecules (Frijhoff et al., Antioxid Redox Signal, 2015). This imbalance is a key driver in the progression of cancer, neurodegeneration, and cardiovascular diseases. Therapeutic strategies aim to restore redox homeostasis by either neutralizing ROS directly or modulating regulatory nodes like the Nrf2-KEAP1 pathway to induce protective gene expression (Tonelli et al., Antioxid Redox Signal, 2018; Robledinos-Antón et al., Antioxidants, 2019).
Modulation of redox homeostasis through direct scavenging of reactive species, inhibition of ROS-generating enzymes like NADPH oxidase, or induction of endogenous antioxidant gene expression via the Nrf2/ARE pathway (Robledinos-Antón et al., Antioxidants, 2019).
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