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Cellular redox pathways encompass the coordinated set of enzymatic and non-enzymatic mechanisms that maintain and regulate the redox state of cells by managing the production, removal, and signaling of reactive molecules such as reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive sulfur species (RSS)[1][8][4]. These pathways involve a wide array of molecules, including NADPH oxidases, antioxidant enzymes (e.g., superoxide dismutase, catalase, glutathione peroxidase, peroxiredoxins), small molecule redox buffers (e.g., glutathione, thioredoxin), and redox-sensitive signaling proteins. Redox signaling is essential for critical cellular functions such as metabolism, proliferation, differentiation, programmed cell death (apoptosis), and stress responses[1][8]. Aberrant regulation of these pathways can contribute to diseases including cancer, neurodegeneration, inflammation, and cardiovascular disorders[3][4][8]. Because "cellular redox pathways" refers to a broad network rather than a single targetable molecule, it does not have a canonical receptor, gene, or protein abbreviation. Therapeutic targeting is possible by modulating key enzymes or regulators within these pathways (e.g., NOX isoforms, glutathione, thioredoxin systems), but such interventions must be precisely controlled to avoid impairment of normal cell signaling and physiology[2][4].
Modulation of redox balance; Inhibition or enhancement of reactive oxygen/nitrogen/sulfur species signaling; Regulation of redox-sensitive transcription factors and enzymes
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