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"Oxidative stress-related pathways" is not a single molecule or canonical drug target but refers collectively to cellular signal transduction and metabolic routes that respond to and regulate reactive oxygen species (ROS) and redox balance. These include major intracellular cascades such as NF-kB, MAPK, PI3K-Akt, and Keap1-Nrf2–ARE signaling. The primary function of these interconnected networks is maintaining redox homeostasis by balancing ROS production—arising from sources like mitochondria and NADPH oxidases—and antioxidant defenses including enzymes such as superoxide dismutase, catalase, glutathione peroxidase, peroxiredoxin, and others. Dysregulation leads to oxidative damage implicated in diverse diseases including cancer, cardiovascular disorders, diabetes mellitus, neurodegeneration, and chronic inflammation. While many drugs modulate elements within these networks—such as antioxidants or inhibitors of NADPH oxidases—the term "oxidative stress-related pathways" does not denote a discrete therapeutic target but rather an umbrella for multiple molecular entities involved in redox regulation.[1][2][3]
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