Investigation of the intracellular signaling induced by the SUMO modification in the process of CHF

阐明衰老和糖尿病作为独立因素促进心肌梗死后心力衰竭的机制，有助于寻找慢性心力衰竭新的治疗靶点。在以往的动物模型报道中，我们发现氧化应激在心力衰竭患者中升高，且氧化应激浓度与心力衰竭的严重程度和预后相关。我们发现DGKalpha在人心脏缺血再灌注损伤过程中具有重要作用，而在小鼠心脏中不存在。我们还发现氧化应激可调节激酶级联反应，并可调节sumo酰化和泛素化，最终引起心肌损伤。

Clarify the mechanisms by which aging and diabetes are independent factor for the advancing the heart failure after myocardial infarction contribute to find a new therapeutic target for chronic heart failure. As shown in previous reports using animal model, we found that oxidative stress is increased in patients with heart failure, moreover, its concentration is associated with the severity and prognosis. We found the important role of DGKalpha, which exist in human heart but not in mice, in the process of ischemia reperfusion injury. We also found that oxidative stress modulated the kinase cascade, and modulated the SUMOylation and ubiquitination, finally induced myocardial injury.