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Cellular redox and reactive oxygen species (ROS) pathways encompass the complex network of biochemical reactions and signaling cascades that maintain the balance between the production of oxidants and their neutralization by antioxidant systems. ROS, including superoxide radicals and hydrogen peroxide, serve as critical secondary messengers in physiological processes such as cell growth, differentiation, and immune activation. However, an imbalance—often termed oxidative stress—leads to the damage of lipids, proteins, and DNA, contributing significantly to the pathogenesis of cancer, neurodegeneration, and cardiovascular diseases. Therapeutic intervention in these pathways involves a diverse array of targets, including enzymes like NADPH oxidases (NOX) and superoxide dismutases (SOD), as well as the master transcriptional regulator Nrf2, which coordinates the cellular antioxidant response. While promising, targeting these pathways is challenging due to the dual role of ROS in both health and disease, requiring precise modulation to avoid disrupting essential homeostatic signaling.
Drugs targeting these pathways typically act by scavenging reactive species, inducing endogenous antioxidant enzymes via Nrf2 activation, or inhibiting ROS-generating enzymes like NADPH oxidases (NOX).
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