Abstract
Release of reactive oxygen species (ROS) generated in the mitochondria to the cytosol is well controlled by various proteins in order to maintain and regulate redox homeostasis and cellular signaling pathways, however, the exact mechanisms by which the proteins located in the mitochondrial membrane control ROS release still remains to be identified. Al though there are reports that several proteins play a role in mitochondrial ROS release to the cytosol, little is known about how it is released into the cytosol or its origin. Recently, several reports demonstrated that the ROS modulator 1 (Romo1) protein located on the mitochondrial membrane modulates ROS release into the cytosol and that these ROS are indispensible for survival in both normal cells and tumor cells. If these ROS are over-produced or dysregulated in pathological conditions, they may cause oxidative damages resulting in a variety of diseases. Therefore, understanding and identifying the mechanisms by which ROS are released to the cytosol may offer new strategies for pharmaceutical therapy of diseases related to oxidative stresses.
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