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. 2015 Jun 12;65(8):1333–1346. doi: 10.1136/gutjnl-2014-308553

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This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited. See: http://creativecommons.org/licenses/by/4.0/

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Summary diagram: the mitochondrial permeability transition pore (MPTP) plays a critical role in the development of acute pancreatitis. Exposure to pancreatic toxins leads to a sustained rise in cytoplasmic calcium that crosses the inner mitochondrial membrane (IMM) to enter the mitochondrial matrix. Consequent cyclophilin D (CypD) activation promotes MPTP opening across the IMM, causing mitochondrial depolarisation and impaired ATP production. These induce PGAM5 activation and retarded autophagy, downstream mechanisms in acute pancreatitis (upper panel). When MPTP opening is inhibited by genetic (Ppif^−/−) or pharmacological means (DEB025 or TR040303), mitochondrial membrane potential is preserved and ATP production sustained. This maintains the integrity of pancreatic acinar cells that clear calcium more effectively and prevents the development of acute pancreatitis (lower panel) (MPTP drawn after reference ¹⁴).