Xu Lab
Dr. Zhelong Xu, MD, PhD, is an Assistant Professor (Tenure Track) and the Director of Cardiovascular Research in the Department of Anesthesiology at the University of North Carolina at Chapel Hill. He is also a faculty member of Carolina Cardiovascular Biology Center. Dr. Xu earned his PhD degree from School of Medicine at Yamagata University in Japan and completed his postdoctoral training in Dr. James M. Downey’s laboratory at the University of South Alabama.
Dr. Xu’s research interests are in the prevention of myocardial ischemia/reperfusion injury. Currently, Dr. Xu’s laboratory is investigating the roles of mitochondria, zinc, and glycogen synthase kinase 3β (GSK-3β) in adenosine A2 receptor activation induced cardioprotection at reperfusion. The experimental approaches that we employ include rat and mouse heart perfusion, molecular and cell biology, confocal imaging, and RT-PCR etc.
Dr. Xu’s research project is supported by the National Institute of Health (NIH). He serves as reviewers for several well-known journals in the field of cardiovascular sciences including Circulation, Cardiovascular Research, Journal of Molecular and Cellular Cardiology, and American Journal of Physiology (Heart and Circulatory Physiology).
Selected Publications
- McIntosh R, Lee S, Ghio AJ, Xi J, Zhu M, Shen, X, Chanoit G, Zvara DA, Xu Z. The critical role of intracellular zinc in adenosine A2 receptor activation induced cardioprotection against reperfusion injury. J Mol Cell Cardiol 2010; 49:41-47.
- Xi J, McIntosh R, Shen X, Lee S, Chanoit G, Criswell H, Zvara DA, Xu Z. Adenosine A2A and A2B receptors work in concert to induce a strong protection against reperfusion injury in rat hearts. J Mol Cell Cardiol 2009; 47: 684-690.
- Lee S, Chanoit G, McIntosh R, Zvara DA, Xu Z. The molecular mechanism underlying Akt activation in zinc-induced cardioprotection. Am J Physiol 2009; 297:H569-H575.
- Chanoit G, Lee S, Xi J, Zhu M, McIntosh RA, Mueller RA, Norfleet EA, Xu Z. Exogenous Zinc Protects Cardiac Cells from Reperfusion Injury by Targeting Mitochondrial Permeability Transition Pore through Inactivation of Glycogen Synthase Kinase 3β. Am J Physiol 2008; 295: H1227-1233.
- Jang YH, Xi J, Wang H, Mueller RA, Norfleet EA, Xu Z. Postconditioning prevents reperfusion injury by activating δ opioid receptors. Anesthesiology 2008; 108: 243-50
- Jang YH, Wang H, Xi J, Mueller RA, Norfleet EA, Xu Z. NO Mobilizes Intracellular Zn2+ via cGMP/PKG Signal Pathway and Prevents Mitochondrial Oxidant Damage in Cardiomyocytes. Cardiovasc Res 2007; 75: 426-43.
- Xu Z, Jang YH, Mueller RA, Norfleet E. IB-MECA and cardioprotection. Cardiovasc Drug Rev 2006; 24: 227-238 (Invited review).
- Park S-S, Zhao H, Jang YH, Mueller RA, Xu Z. IB-MECA confers cardioprotection at reperfusion by inhibiting mitochondrial permeability transition pore opening via glycogen synthase kinase 3β. J Pharm Exp Ther 2006; 318: 124-13.
- Park S-S, Zhao H, Mueller RA, Xu Z. Bradykinin prevents myocardial reperfusion injury by inhibiting GSK-3β and MPTP opening. J Mol Cell Cardiol. 2006; 40: 708-71.
- Xu Z, Mueller RA, Park S-S, Boysen PG, Cohen MV, Downey JM. Cardioprotection with adenosine A2 receptor activation at reperfusion. J Cardiovasc Pharmacol 2005; 46:794-802 (Review paper).
- Xu Z, Park S-S, Mueller RA, Bagnell RC, Patterson C, Boysen PG. Adenosine produces nitric oxide and prevents mitochondrial oxidant damage in rat cardiomyocytes. Cardiovasc Res 2005;65: 803-812.
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