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

阐明衰老和糖尿病是心肌梗死后心力衰竭进展的独立因素的机制，有助于寻找治疗慢性心力衰竭的新靶点。如以往的动物模型报道所示，我们发现心力衰竭患者体内氧化应激水平升高，且其浓度与心力衰竭的严重程度及预后有关。我们发现DGKalpha在缺血再灌注损伤过程中起着重要作用，它存在于人的心脏而不存在于小鼠。我们还发现，氧化应激调节了激酶的级联，并调节了SUMO化和泛素化，最终导致了心肌损伤。

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.