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Figure 3: TSPO is a therapeutic target for arrhythmia, myocardial infarction, and cardiac hypertrophy. Ischemia/reperfusion rapidly induces reactive oxygen species (ROS) production from the electron transport chain, and ROS are released to mitochondrial matrix. A local burst of mitochondrial ROS leads to the increase of ROS production and oscillations in mitochondrial membrane potential ( ), which can destabilize neighboring mitochondrial membrane by inducing the release of ROS. The collapses of are regulated by inner membrane anion channels (IMACs) opening, which is key in the genesis of arrhythmia. The burst of ROS in cellular matrix activates a broad variety of signaling kinases and transcription factors related to cardiac hypertrophy. The imbalance of IMAC influences the opening of mitochondrial permeability transition pore (mPTP), leading to the release of cytochrome c and activation of caspase cascade, and contributes to myocardial infarction. Targeting TSPO can reverse the above changes. Thus, TSPO is a therapeutic target for arrhythmia, myocardial infarction, and cardiac hypertrophy through reducing ROS.