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The mitochondrial bioenergetic pathway encompasses the integrated network of protein complexes and metabolic reactions within the mitochondrion responsible for generating ATP via oxidative phosphorylation, as well as related processes such as substrate transport, TCA cycle function, and regulation of redox status[1][3][7]. These pathways include the electron transport chain (complexes I–IV), ATP synthase (complex V), mobile electron carriers (ubiquinone, cytochrome c), and associated substrate shuttles. Disruption or modulation of these pathways is central to many diseases, including cancer, neurodegeneration, and metabolic disorders, and such pathways are indirectly targeted by a variety of drugs either to enhance resilience or to selectively induce apoptosis in diseased cells[3][4][6]. "Mitochondrial bioenergetic pathways" is not a standard, actionable molecular drug target like a receptor, enzyme, or transporter, but describes a complex system integral to cell functioning and disease mechanisms. Targeting "the pathway" typically means modulating one or more constituent proteins or enzyme complexes (such as specific ETC complexes, transporters, and regulatory enzymes)[1][3][4].
Antioxidant action (ROS scavenging); ETC complex inhibition or modulation; NAD+/NADH modulation; Induction or inhibition of apoptosis; Modulation of oxidative phosphorylation
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