Mitochondrial dysfunction is central to the pathogenesis of acute pancreatitis as well as other diseases including ischemia-reperfusion injury of the heart, brain and kidney, muscular dystrophies and neurodegeneration.
Mitochondrial dysfunction is the result of a sudden increase in permeability of the inner mitochondrial membrane (IMM), via persistent opening of a multi-protein channel known as the mitochondrial permeability transition pore (MPTP) . This allows uncontrolled proton flow across the IMM and unregulated flux of water, ions and solutes up to 1.5 kDa into and out of the mitochondrial matrix.
This results in loss of inner mitochondrial-membrane potential, which is essential for ATP production, disruption of calcium homeostasis, swelling of mitochondria and of the outer mitochondrial membrane (OMM). Eventually cells start dying through necrosis in an uncontrolled manner.
Therefore, MPTP could be an attractive target for maintenance of mitochondrial function and cell death prevention in a host of disease states.
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