Laboratory of Intracellular Ion Channels, Nencki Institute of Experimental Biology, Polish Academy of Sciences, 02-093 Warsaw, Poland.
Department of Histology, Medical University of Gdansk, 1a Debinki, 80-211 Gdansk, Poland.
Molecules. 2022 Jan 4;27(1):299. doi: 10.3390/molecules27010299.
Mitochondrial potassium channels control potassium influx into the mitochondrial matrix and thus regulate mitochondrial membrane potential, volume, respiration, and synthesis of reactive oxygen species (ROS). It has been found that pharmacological activation of mitochondrial potassium channels during ischemia/reperfusion (I/R) injury activates cytoprotective mechanisms resulting in increased cell survival. In cancer cells, the inhibition of these channels leads to increased cell death. Therefore, mitochondrial potassium channels are intriguing targets for the development of new pharmacological strategies. In most cases, however, the substances that modulate the mitochondrial potassium channels have a few alternative targets in the cell. This may result in unexpected or unwanted effects induced by these compounds. In our review, we briefly present the various classes of mitochondrial potassium (mitoK) channels and describe the chemical compounds that modulate their activity. We also describe examples of the multidirectional activity of the activators and inhibitors of mitochondrial potassium channels.
线粒体钾通道控制钾离子流入线粒体基质，从而调节线粒体膜电位、体积、呼吸和活性氧物质 (ROS) 的合成。已经发现，在缺血/再灌注 (I/R) 损伤期间，药理学上激活线粒体钾通道会激活细胞保护机制，导致细胞存活率增加。在癌细胞中，这些通道的抑制会导致细胞死亡增加。因此，线粒体钾通道是开发新的药理学策略的有趣靶点。然而，在大多数情况下，调节线粒体钾通道的物质在细胞中还有其他几个替代靶点。这可能导致这些化合物引起意外或不必要的作用。在我们的综述中，我们简要介绍了各种类型的线粒体钾 (mitoK) 通道，并描述了调节其活性的化学化合物。我们还描述了线粒体钾通道激活剂和抑制剂的多向活性的例子。
