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Calcium overload of mitochondria leads to their damage after a heart attack (ischaemia and reperfusion) via opening of the mitochondrial permeability transition pore. This is caused by large calcium oscillations in cardiac myocytes which result in mitochondrial calcium overload. NAADP is the most powerful activator of calcium release, and is known to induce calcium oscillations in various cell types. We showed here that NAADP contributes to these lethal Calcium oscillations at reperfusion, and that using an inhibitor of NAADP activated channels (TPC1) or TPC1 knockout mice, that this reduces cardiac injury.
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This page is a summary of: Inhibition of NAADP signalling on reperfusion protects the heart by preventing lethal calcium oscillations via two-pore channel 1 and opening of the mitochondrial permeability transition pore, Cardiovascular Research, September 2015, European Society of Cardiology,
DOI: 10.1093/cvr/cvv226.
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