Research for heart failure by regulating mitochondrial energy metabolism with p53

缺血或高血糖诱导心脏P53、SCO2(细胞色素c氧化酶2的合成)和TIGAR(TP53诱导的糖酵解和凋亡调节因子)。我们证实了糖尿病引起的SCO2，从而促进了心脏脂肪毒性(循环心力衰竭)。2012年)。缺血诱导P53和TIGAR，抑制糖酵解(Am J Physiol心脏循环Physiol.2010)和心肌中的有丝分裂吞噬(J摩尔细胞心脏)。2012年)。我们还发现，P53/TIGAR介导的抑制心肌细胞有丝分裂与心肌梗死后的心室重构有关(J Mol Cell心脏ol 2012)。SCO2杂合子小鼠对糖尿病心肌病有保护作用。这些数据表明，调节能量代谢将是治疗心力衰竭的一种新疗法。

Ischemia or hyperglycemia induced p53, SCO2(Synthesis of cytochrome c oxidase 2) and TIGAR(TP53-induced glycolysis and apoptosis regulator) in the heart. We demonstrated diabetic condition induced SCO2, which promoted cardiac lipotoxicity(Circ Heart Fail. 2012). Ischemia induced p53 and TIGAR, which inhibited glycolysis(Am J Physiol Heart Circ Physiol. 2010) and mitophagy in the myocardium(J Mol Cell Cardiol. 2012). We also found that p53/TIGAR-mediated inhibition of myocyte mitophagy was responsible for ventricular remodeling after myocardial infarction.(J Mol Cell Cardiol 2012). SCO2 heterozygote mice were protective against diabetes induced cardiomyopathy. These data indicated that regulating energy metabolism will be a novel therapeutics for heart failure.