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. 2020 Aug 17;9(8):760. doi: 10.3390/antiox9080760

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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BK_Ca signaling in cardiomyocytes mitochondria during ischemia-reperfusion (I/R) injury. I/R injury causes an increase of reactive oxygen species (ROS) production and Ca²⁺ overload that leads to mPTP opening, the collapse of membrane potential (ΔΨ_IMM), and the release of cytochrome C that causes cell death. The opening of BK_Ca protects the heart by reducing ROS and increasing the calcium retention capacity, hence delaying the opening of mPTP. IMM—Inner mitochondria membrane, OMM—Outer mitochondria membrane. mitoBK_Ca activators (NS1619, NS11021), mitoBK_Ca inhibitors (PAX-paxilline, IbTX-iberiotoxin), mPTP-mitochondrial permeability transition pore.