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The mitochondrial permeability transition pore (MPTP) is a large conductance channel that forms in the inner mitochondrial membrane under pathological conditions, leading to increased permeability and mitochondrial dysfunction. Its opening can trigger cell death via necrosis or apoptosis. The precise molecular composition remains incompletely defined, but F-ATP synthase is a likely core component. Key regulators include calcium ions, reactive oxygen species, and adenine nucleotides. MPTP plays a central role in ischemia-reperfusion injury, neurodegeneration, and other diseases. Therapeutic targeting is focused on developing selective modulators to inhibit inappropriate activation.
Cyclosporin A inhibits MPTP opening by binding to cyclophilin D.
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