Moravec

Christine Schomisch Moravec, Ph.D.

Assistant Staff

Dept. of Molecular Cardiology
Cleveland Clinic Heart Center / FF20
9500 Euclid Avenue
Cleveland, Ohio, 44195
Telephone: (216) 445-9949
Fax: (216) 445-9951
moravec@ccf.org

Area of general research interest:

human heart failure, intracellular signaling, calcium cycling, myocardial contractility

Investigators:

  • Christine Moravec, Ph.D.
  • Nicholas R DiPaola, Ph.D.
  • Monique L Ogletree-Hughes, Ph.D.
  • Nancy DiIulio, Ph.D.
  • Rosalia Matteo, Ph.D.
  • Wendy Sweet, M.S.
  • Louise Aquila-Pastir, M.S.
  • Cassandra Talerico, M.A.

Collaborators:

  • Patrick McCarthy, M.D.
  • Nicholas Smedira, M.D.
  • James B Young, M.D.
  • Randy Starling, M.D.
  • Gary Francis, M.D.
  • Norman B Ratliff, M.D.
  • David Van Wagoner, Ph.D.
  • Vincent K Tuohy, Ph.D.
  • Robert Fairchild, Ph.D.
  • Meredith Bond, Ph.D.

Brief Description:

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.

Key References:

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.