Cardiovascular Center of Excellence

Research

The Cardiovascular Center at the University of Cincinnati College of Medicine has a long-standing tradition of cardiovascular research excellence. The current faculty comprises the CVC nucleus of our entire campus and leads the UC Medical Center in funding levels and productivity. The CVC faculty consists of an extremely collaborative and collegial group that is all contained within a 3 building span no more than 200 meters from a center point. The group has been recognized by its extraordinary productivity and national as well as international stature.

SPECIFIC FOCUSS AREAS OF RESEARCH

• Ashraf M. - Elucidate the subcellular & molecular mechanisms of ischemia/reperfusion injury in the myocardium and its prevention by therapeutic interventions
• Davidson W. - Understanding how the structure and compostition of high density lipoproteins contributes to their protection from cardiovascular disease
• Fan G. - Elucidate the functional significance of microRNA and Hsp20 in cardioprotection
  
• Hui D. - relating cholesterol metabolism with individual susceptibility for coronary heart disease
  
• Jones W. - elucidation, at the molecular level, of the signal transduction and gene regulatory events that underlie the development of cardiovascular pathophysiology
  
• Kranias E. - elucidate the regulatory mechanisms and signaling pathways underlying calcium homeostasis in cardiac muscle and the alterations in these pathways underlying the heart failure phenotype
  
• Lingrel J. - pattern of gene expression during development of several tissues including lung, kidney, heart, T cells, and endothelial vascular cells
  
• Lorenz J. - the study of integrative physiology in a variety of genetically altered mice produced at UC and elsewhere
  
• Matlib M. - Modulation of acyl-CoA thioesterase-2 (ACOT2) for up-regulation of long-chain fatty acid oxidation in mitochondria as a novel therapeutic approach for prevention of lipid accumulation and treatment of lipotoxicity and heart failure in obesity and diabetes.
  
• Herr A. - Structural and biophysical studies of cellular adhesion and receptor activation, focusing on thrombosis, bacterial pathogenesis, and antibody-mediated immune responses
• Menon A. - Normalcy and disease in the cardiovascular system
• Hui D. - Relating cholesterol metabolism with individual susceptibility for coronary heart disease
  
• Millard R. - cardiac muscle receptors and cytoskeletal proteins, programmed cell death molecules, and the regulation of norepinephrine release and recovery by adrenergic nerves
  
• Molkentin J. - Molecular basis of early and late cardiac disease
  
• Rapoport R. - regulation of the cerebral vasculature, with an emphasis on elucidating the mechanisms underlying the vasospasm following 1) subarachnoid hemorrhage, 2) hypocapnia, and 3) cocaine
• Ren X.- Focus on elucidating the molecular and neural mechanisms of non-ischemic remote preconditioning by nociceptive stimulation
  
• Robbins J. - Dr. Robbins works on modifying the genetic complement of mice and rabbits in an attempt to explore function-structure relationships that underlie normal cardiovascular function and heart disease.
  
• Shull G. - To understand the physiological functions of epithelial ion transporters and calcium pumps in both health and disease
  
• Schultz J. - (1) Identify and characterize signaling events involved in protecting the myocardium from ischemic injury and cell death following myocardial infarction (i.e., heart attack) and 2) Determine the mechanisms by which cardiac hypertrophy and heart failure occur following myocardial infarction or hemodynamic load (high blood pressure or volume overload)
  
• Wang H. - understand the properties, functions and regulation of physiologically important ion channels in two systems, cardiac muscle cells and the nervous system
  
• Weintraub N. - Mechanisms of inflammation in atherosclerosis and heart disease
  
• Wieczorek D. - (1) the functional significance for the production of different tropomyosin isoforms in vertebrates; and (2) the structural, physiological, and molecular effects on the heart following overexpression or ablation of normal or disease-associated tropomyosins.

Focus Group
Members

Ashraf, M

Davidson, W

Collins, S

Fan, G

Haider, K

Herr, A

Hui, D

Jones, W K

Kranias, E

Lingrel, J B

Lorenz, J N

Matlib, M

Menon, A

Millard, R

Miller, W

Molkentin, J

Rapoport, R

Ren, X

Robbins, J

Rothenberg, F

Schultz, J

Shull, G

Stern, D

Tso, P

Wang, HS

Weintraub, N

Wieczorek, D

Xu, M