Mitochondrial K (ATP) Channels Opening: Pathways of Cytoprotection- Juniper Publishers


JUNIPER PUBLISHERS-OPEN ACCESS JOURNAL OF TOXICOLOGY

Mitochondrial K (ATP) Channels Opening: Pathways of Cytoprotection


Authored by Olga V Akopova

Abstract

Mitochondrial K (ATP) channels (mKATP channels) opening was shown to be cytoprotective under different pathophysiological conditions. Generally it was supposed that the modulation of ROS and RNS production could largely explain antiapoptotic and cytoprotective effects afforded by pharmacological mK(ATP) channels openers. But how to explain cytoprotection regardless of contradictory effects of mKATP channels opening on ROS production in mitochondria? Relying on published data, we try to answer this question there.

Mitochondrial ROS and RNS overproduction have a great cytotoxic potential well described in the literature. Several pathophysiological conditions and the action of cytotoxic agents are accompanied by excess ROS and RNS formation. These free radical products and their derivatives could easily modify cellular proteins, lipids, channels and enzymes and trigger multiple cell death pathways. Most dangerous is the interplay between ROS and RNS resulting in the formation of highly toxic products, such as •OH radical and peroxynitrite. Their excess formation is known to severely aggravate pathophysiological conditions. mKATP channels openers were shown to be effective in prevention of apoptosis and necrosis under different pathological states, but, regardless of extensive studies of last two decades, pathways of their cytoprotective action are poorly understood. The progress is essentially hampered by still unknown molecular composition of mKATP channels.

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