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Christine Schomisch Moravec, Ph.D.Associate Staff
Dept. of Molecular Cardiology
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human heart failure, autonomic nervous system, heart disease in women, psychophysiology
Collaborators:
As Director of Basic Research in the Kaufman Center for Heart Failure (within the Department of Cardiovascular Medicine), research in my laboratory focuses on human heart failure (HF), using two different approaches.
First, we attempt to understand physiological, cellular, and biochemical changes during HF and whether these changes can be reversed by therapies such as a left ventricular assist device (LVAD) or β-adrenergic receptor blockers. We collaborate with clinical colleagues to obtain patient information and perform laboratory studies on tissue samples at the time of transplantaions with LVAD or hearts. Ongoing NIH funding focuses on the JAK-STAT signaling pathway and its role in human HF. A new NIH grant application concerns the functional role of β-2 receptor upregulation following LVAD implantation.
We also investigate the role of psychophysiologic remodeling in HF, using biofeedback-assisted stress management and testing the hypothesis that this type of intervention can also affect the cellular and molecular phenotype in HF patients by interfering with overactivation of the sympathetic nervous system. Our goal is to demonstrate that biologic remodeling of the failing heart following a psychophysiologic intervention. These projects are funded by the American Heart Association and Cleveland Clinic’s Bakken Heart-Brain Institute.
The newest project in our laboratory tests the effects of several different stress management techniques in patients with coronary artery disease, again using biologic and clinical endpoints.
McGafin KR, Moravec CS, McTiernan CF. Leptin signaling in the mailing and mechanically unloaded heart. Circulation Heart Failure 2009: 676-683.
Prasad SVN, Duan ZH, Gupta MK, Surampudi SK, Volinia S, Calin GA, Kotwal A, Moravec CS, Starling RC, Perez DM, Sen S, Wu Q, Plow EF, Croce CM, Karnik S. A unique microRNA profile in end-stage heart failure indicates alterations in specific cardiovascular signaling networks. J Biol Chem 2009; 284:27487-27499.
Moravec CS. Biofeedback therapy in cardiovascular disesae: rationale and research overview. Cleve Clin J Med 75:S35-S38, 2008.
Pilbrow AP, Ellmers LJ, Black M, Moravec CS, Sweet WE, Troughton RW, Richards AM, Frampton CM, Cameron VA. Genomic selection of reference genes for real-time PCR in human myocardium. BMC Medical Genomics 2008: 1:64.
Fedak PW, et al. Altered expression of disintegrin metalloproteinases and their inhibitor in dilated cardiomyopathy. Circulation 2006;113:238-45.
Aquila LA, et al. Cytoskeletal structure and recovery in single human cardiac myocytes. J Heart Lung Transplant 2004;23:954-63.
Tan FL, et al. The gene expression fingerprint of human heart failure. Proc Natl Acad Sci 2002; 99:11387-92.
Ogletree-Hughes ML, et al. Mechanical unloading restores β-adrenergic responsiveness and reverses receptor downregulation in the failing human heart. Circulation 2001;104:881-6.