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Cellular reductases and mitochondrial redox systems represent a diverse group of enzymes and metabolic pathways that maintain the electrochemical balance within cells and drive ATP production. This target class includes the mitochondrial electron transport chain (ETC) complexes, as well as the glutathione and thioredoxin antioxidant systems, which are essential for neutralizing reactive oxygen species (ROS) generated during respiration [1, 2]. These systems play a dual role in physiology: they are vital for energy metabolism and cellular signaling, but their dysfunction is a primary driver of oxidative stress and mitochondrial decay [3]. In oncology, these systems are often targeted to disrupt the metabolic adaptations of tumor cells, while in neurodegeneration, the goal is typically to enhance redox capacity to prevent neuronal death [4]. Drugs interacting with these systems range from metabolic modulators like metformin to direct antioxidants and respiratory inhibitors [5].
Inhibition of mitochondrial complex I, modulation of cellular redox potential, scavenging of reactive oxygen species, and replenishment of antioxidant pools.
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