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Reactive oxygen species (ROS) and redox-related pathways encompass the biochemical processes involved in the generation, signaling, and neutralization of oxygen-derived molecules such as superoxide and hydrogen peroxide (NIH, 2015). In physiological conditions, ROS act as vital secondary messengers that regulate cell growth, differentiation, and immune responses (Antioxid. Redox Signal., 2015). However, an imbalance between ROS production and the body's antioxidant capacity—termed oxidative stress—leads to macromolecular damage to DNA, proteins, and lipids, contributing to the pathogenesis of cancer, neurodegeneration, and cardiovascular diseases (J. Clin. Invest., 2026). Therapeutic strategies focus on restoring redox homeostasis by either neutralizing excess ROS with antioxidants or enhancing endogenous defenses through Nrf2 activation (NIH, 2026). Despite their potential, targeting these pathways is challenging because ROS are essential for normal signaling, and global suppression can lead to unintended side effects or even promote disease progression in certain contexts (ResearchGate, 2026). Biomarkers such as 8-hydroxy-2'-deoxyguanosine and malondialdehyde are commonly used to monitor oxidative damage and treatment efficacy (ACS, 2015).
Modulation of redox balance through direct antioxidant scavenging, activation of the Nrf2-Keap1 antioxidant response pathway, or pharmacological inhibition of ROS-generating enzymes such as NADPH oxidases (NOX), xanthine oxidase (XO), and monoamine oxidase (MAO).
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