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Reactive oxygen species (ROS)-related oxidative pathways encompass the biochemical processes involved in the generation, signaling, and neutralization of oxygen-derived free radicals and non-radical oxidants within a cell (Sies et al., 2017). Under physiological conditions, ROS serve as critical signaling molecules in processes such as cell proliferation, differentiation, and immune defense (Pizzino et al., 2017). However, an imbalance between ROS production and the capacity of antioxidant systems leads to oxidative stress, which causes damage to DNA, proteins, and lipids (He et al., 2020). This oxidative damage is a hallmark of various pathologies, including cancer, neurodegenerative disorders, and cardiovascular diseases (Forman & Zhang, 2021). Therapeutic strategies targeting these pathways often focus on enhancing antioxidant defenses or inhibiting specific ROS-generating enzymes to restore redox homeostasis (Pizzino et al., 2017). Because ROS are essential for normal cellular functions, therapeutic interventions must be carefully calibrated to avoid interfering with necessary physiological signaling (Forman & Zhang, 2021).
Modulation of redox homeostasis through ROS scavenging, inhibition of ROS-generating enzymes (e.g., NADPH oxidase), or induction of antioxidant gene expression via the Nrf2-KEAP1 pathway.
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