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Hina W. Chaudhry

Hina Chaudhry
Hina W.
Chaudhry
M.D.
Associate Professor of Medicine
Mount Sinai School of Medicine
Director of Cardiovascular Regenerative Medicine
hina.chaudhry@mssm.edu

Dr. Chaudhry's research focuses on cardiac regeneration, the role of cell cycle regulation of cardiomyocytes and endogenous cardiac progenitor cells. Chaudhry's lab has found that cyclin A2 is a critical gene mediating cardiomyocyte mitoses even after birth when expressed in the heart of transgenic mice. After a myocardial infarction (MI) is induced, these mice are able to repair their hearts with significantly restored cardiac function. There is molecular and cellular evidence of "de novo" cardiogenesis. The formation of new cardiomyocytes appears to involve side-population (SP) stem cells which may be differentiating into cardiomyocytes after injury is induced. As a translational strategy, the lab has delivered cyclin A2 cDNA in an adenoviral vector to adult, genetically naive rat hearts after MI, and observed significant restoration of cardiac function with evidence of cardiomyocyte proliferation. Present and future goals include investigations of the mechanisms of proliferation observed in these two, distinct small animal models and extending these studies into large animals with subsequent human clinical trials.

Select Publications: 

Cheng RK, Asai T, Tang H, Dashoush NH, Kara RJ, Costa KD, Naka Y, Wu EX, Wolgemuth DJ, Chaudhry HW: Cyclin A2 Promotes Cardiac Regeneration after Myocardial Infarction and Prevents Heart Failure. Circulation Research, 2007 Jun 22;100(12):1741-8. original article and cover figure.

Woo YJ, Panlilio CM, Cheng RK, Liao GP, Atluri P, Cohen JE, Chaudhry HW: Therapeutic Delivery of Cyclin A2 Induces Myocardial Regeneration and Enhances Cardiac Function in Ischemic Heart Failure. Circulation, 2006;114:I-206  I-213.

Chaudhry HW, Dashoush N, Tang H, Zhang L, Wang X, Wu EX, Wolgemuth DJ: Cyclin A2 Mediates Cardiomyocyte Mitosis in the Postmitotic Myocardium. Journal of Biological Chemistry, Aug 20 2004; 279 (34): 35858-35866.