Reducing ischemia reperfusion (I/R) injury has been a major challenge in the treatment of cardiovascular disease. It is widely accepted that mitochondrial apoptosis is an important link in myocardial infarction induced by I/R damage. Studies suggested that aryl hydrocarbon receptor (AhR) pathway plays an important role in the development and function of the cardiovascular system and regulating the mitochondrial homeostasis. AhR played a critical role in regulating mitochondrial homeostasis in response to TCDD-induced stress through translocation of AhR from the cytoplasm into the cell nucleus. And a portion of AhR was found in the mitochondrial inter membrane space. Moreover, there were abundant AhR expression in myocardial cells induced by I/R, and ischaemic post-conditioning reversed apoptotic reperfusion injury involving the AhR signaling pathway. Additionally, AhR is involved in the mechanism of cardiac toxicity of many chemotherapeutic agents. Given the discovery mentioned above, we hypothesize that AhR pathway participates in myocardial ischemia reperfusion injury by regulating mitochondrial apoptosis. Meanwhile, how the AhR pathway is involved in I/R damage and regulating mitochondrial apoptosis is needed to further verified. To evaluate our hypothesis, we will measure the expression of AhR in mitochondria and cytoplasm after myocardial ischemia and reperfusion in vitro and in vivo. And then study the AhR pathway in regulating mitochondrial apoptosis to participate in myocardial I/R injury using mitochondrial protein mass spectrometry analysis and RNA interference technique. If our hypothesis is correct, AhR will be a key target in myocardial I/R injury and myocardial infarction, which could provide important agents.