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Mitochondrial pathways encompass a diverse array of biochemical processes essential for cellular energy production, metabolic homeostasis, and programmed cell death. The primary function of these pathways is the generation of adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS), alongside the regulation of the tricarboxylic acid (TCA) cycle and fatty acid oxidation [1, 2]. Beyond energy production, mitochondria serve as central hubs for apoptosis via the release of cytochrome c and the regulation of BCL-2 family proteins [3]. Dysfunction within these pathways is a hallmark of numerous pathologies, including neurodegenerative diseases like Parkinson's, where impaired respiratory chain activity leads to oxidative stress, and cancer, where metabolic reprogramming supports tumor growth [4, 5]. Therapeutic intervention in mitochondrial pathways includes the use of Metformin to inhibit Complex I for type 2 diabetes and Venetoclax to target mitochondrial-associated BCL-2 in hematologic malignancies [6, 7].
Modulation of the electron transport chain, regulation of the mitochondrial permeability transition pore (mPTP), and activation or inhibition of mitochondrial-mediated apoptotic signaling.
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