There are two main lines of research work in the lab.  One is to understand the functional significance of altered substrate metabolism in the heart using transgenic mice in combination with multi-nuclei NMR techniques.  This line of research seeks to generate a basis for metabolic therapy for heart failure and cardiac lipotoxicity in obesity and diabetes. Another line of research focuses on metabolic signaling in the heart. We were the first to report an increased activity of AMPK-activated protein kinase (AMPK), an energy sensor and master switch of metabolism, in hypertrophied hearts; and subsequently generated mice with cardiac-specific kinase-dead AMPK.  We are now investigating novel roles of AMPK in mitochondria function, cell growth and insulin sensitivity.  Furthermore, we have been studying the mechanisms linking aberrant AMPK activity due to mutations of gamma-2 regulatory subunit of AMPK and the development of cardiomyopathy with excessive glycogen accumulation.

Selected publications：

1.    Luptak I, Balschi JA, Xing Y, Leone TC, Kelly DP, Tian R. Decreased contractile reserve in PPARa-null hearts can be rescued by increasing glucose transport and utilization. Circulation 2005; 112:2339-2346.

2.         Zou L, Shen M, Arad M, He H, Lofgren B, Ingwall JS, Seidman CE, Seidman JG, Tian R. N488I mutation of the g2-subunit results in bi-directional changes in AMPK activity.  Circ Res 2005; 97(4):323-328.

3.        Tian R, Balschi JA. Interaction of insulin and AMPK in the ischemic heart: Another chapter in the book of metabolic therapy?  Circ Res 2006; 99:3-5.

4.        Luptak I, Shen M, He H, Hirshman MF, Musi N, Goodyear LJ, Yan J, Wakimoto H, Morita H, Arad M , Seidman CE, Seidman JG, Ingwall JS ,Balschi JA, Tian R.  Aberrant activation of AMP-activated protein kinase remodels metabolic network in favor of cardiac glycogen storage. J Clin Invest. 2007,117(5):1432-9.

5.         Luptak I, Yan J, Cui L, Jain M, Liao R, Tian R. Long-term effects of increasing glucose entry on mouse hearts during normal aging and ischemic stress. Circulation, in press.

热忱欢迎参加！