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Reactive oxygen species (ROS)-mediated cellular pathways encompass a complex network of biochemical signaling events triggered by oxygen-derived molecules such as superoxide, hydrogen peroxide, and hydroxyl radicals (PMID: 28138081). While traditionally viewed as harmful byproducts of aerobic metabolism, ROS are now recognized as critical secondary messengers that regulate essential physiological processes, including cell growth, differentiation, and the innate immune response (PMID: 30116495). An imbalance between the production of ROS and the cellular antioxidant defense systems leads to oxidative stress, which is a primary driver in the pathogenesis of cancer, neurodegenerative disorders like Alzheimer's disease, and cardiovascular conditions (PMID: 23603008). Therapeutic strategies often focus on modulating these pathways through the use of antioxidants to scavenge radicals or by activating the Nrf2-Keap1 system to enhance endogenous antioxidant enzyme expression (PMID: 25653194). However, because ROS are necessary for normal cellular signaling, pharmacological interventions must be precisely targeted to avoid interfering with vital homeostatic functions, a challenge often referred to as the antioxidant paradox (PMID: 24591657).
Modulation of redox-sensitive transcription factors (e.g., Nrf2), direct scavenging of free radicals, and inhibition of ROS-generating enzymes such as NADPH oxidases (PMID: 25653194).
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