Research for heart failure by regulating myocardial energy metabolism with p53 and TIGAR.

我们证明了p53和TIGAR抑制缺氧肌细胞的糖酵解，糖酵解的抑制与细胞凋亡密切相关，这表明p53和TIGAR是缺血应激下细胞能量稳态和细胞死亡的重要介质。[J] .中华心脏杂志，1999,19(3):391 - 391。H1916, 2010)。我们还发现，p53/ tigar介导的肌细胞线粒体自噬抑制是导致线粒体完整性受损和随后的细胞凋亡的原因，这一过程与心肌梗死后p53介导的心室重构密切相关。[J] .中国生物医学工程学报；21(2):481 - 481,2012。

We demonstrated that p53 and TIGAR inhibit glycolysis in hypoxic myocytes and that inhibition of glycolysis is closely involved in apoptosis, suggesting that p53 and TIGAR are significant mediators of cellular energy homeostasis and cell death under ischemic stress.(Am J Physiol Heart Circ Physiol 299 : H1908.H1916, 2010.) We also found that p53/TIGAR-mediated inhibition of myocyte mitophagy is responsible for impairment of mitochondrial integrity and subsequent apoptosis, the process of which is closely involved in p53-mediated ventricular remodeling after myocardial infarction.(J Mol Cell Cardiol.; 52 : 175-184, 2012) Approache to control p53/TIGAR signal is important to develop novel therapeutics for heart failure.