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Cellular redox and oxidative stress pathways represent a complex network of biochemical processes that regulate the balance between reactive oxygen species (ROS) production and antioxidant defenses (Sies & Jones, 2020, Nature Reviews Molecular Cell Biology). These pathways are essential for maintaining cellular homeostasis, where low levels of ROS act as secondary messengers in signal transduction, cell proliferation, and immune responses (Pizzino et al., 2017, Oxidative Medicine and Cellular Longevity). When the production of ROS exceeds the capacity of antioxidant systems—such as superoxide dismutase, catalase, and the glutathione system—oxidative stress occurs, leading to oxidative damage of DNA, proteins, and lipids (Forman & Zhang, 2021, Nature Reviews Drug Discovery). This imbalance is a hallmark of various pathologies, including cancer, neurodegenerative diseases like Alzheimer's, and cardiovascular disorders (Hayes & Dinkova-Kostova, 2014, Trends in Biochemical Sciences). Pharmacological intervention typically targets specific nodes within these pathways, such as the Nrf2-Keap1 axis to upregulate endogenous antioxidants or the inhibition of NADPH oxidases (NOX) to reduce ROS generation (Sies & Jones, 2020). However, therapeutic development is complicated by the dual nature of ROS, as excessive suppression can lead to reductive stress and impair vital physiological signaling (Forman & Zhang, 2021).
Modulation of redox balance through the scavenging of reactive oxygen species, activation of antioxidant transcription factors such as Nrf2, or the inhibition of ROS-generating enzymes like NADPH oxidase.
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