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Redox pathways refer to the complex networks regulating oxidation–reduction reactions in biological systems. These pathways coordinate the production and elimination of reactive species (like reactive oxygen species and reactive nitrogen species), control redox-sensitive signaling, and modulate enzyme and protein activity via reversible oxidation of key amino acid residues such as cysteine[1][2][3]. Major molecular players include enzymes (e.g., NADPH oxidases, superoxide dismutases, catalase, glutathione peroxidase), small molecule antioxidants (e.g., glutathione, ascorbate), and thiol redox switches in proteins. Redox homeostasis is central to normal cell function, including metabolism, differentiation, and response to environmental and physiological stimuli. Disruption of these pathways—either excess ROS production (oxidative stress) or inadequate signaling—can contribute to pathologies ranging from cancer and neurodegeneration to inflammation and metabolic syndromes. "Redox pathways" is a functional concept rather than a single protein or receptor, and thus, is not typically considered a direct molecular drug target[1][2][3].
Modulation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) production; Targeting redox-sensitive proteins (such as thiol switches); Induction or inhibition of antioxidant responses (e.g., NRF2 pathway activation); Direct scavenging of free radicals
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