The Independence Blue Cross Cardiovascular Research Center (CVRC) is a consortium of basic and clinical scientists with a broad mission to develop new knowledge that will lead to better understanding of the causes of cardiovascular diseases. Operationally, the CVRC facilitates multilevel, interdisciplinary collaborations that help target basic research towards clinical challenges and enables translation of discoveries into novel approaches for the detection, treatment and prevention of debilitating cardiovascular disorders. Our major research themes at present are:
- Cellular and molecular bases of human heart failure
- Pathophysiology of cardiac structural and functional remodeling after myocardial infarction.
- Biology of proliferative arteriopathy (restenosis and allograft arteriopathy)
- Transplant immunology and allograft vasculopathy
- Endothelial modulation of vascular tone
- Hypertension: Fundamental mechanisms and strategies for reversal
- Stem cells and cardiac repair.
- Cardiac hypertrophy
- Immunology and cardiac disease
- Microvascular function in health and disease
- Atrial function in health and disease
- Atrial fibrillation
- Cardiac development and heart disease.
- Congestive heart failure
- Cardiac metabolism
- Metabolic syndrome, diabetes and cardiovascular disease
CVRC investigators employ a wide spectrum of in vitro techniques, relevant animal models and patient-based research methods. Research is conducted within a new medical research building at the Lewis Katz School of Medicine. CVRC core laboratories supply investigators with small and large animal models of cardiovascular disease for their studies. Open laboratory space enhances collaboration and the student/fellow experience.
Houser Laboratory Research Interest
The research in the Houser laboratory is focused on those processes that maintain the electrical and contractile properties of the normal heart and the defects in these processes that lead to electrical instability (arrhythmias and sudden death) and poor cardiac pump performance congestive heart failure). We are currently continuing our studies of the determinants of cellular electrical and mechanical defects in diseased cardiac myocytes. In addition, we are exploring the idea that a major factor that determines the overall state of cardiac myocyte function is a balance between new myocyte formation (cardiac regeneration) and programmed myocyte death (apoptosis).
Our cell physiology studies are exploring the idea that activation of Ca2+ dependent signaling pathways (mainly through CAMKII) regulates Ca2+ handling proteins in diseased myocytes. We have developed techniques in live cells to track Ca2+ dependent activation of NFAT and are characterizing the associated alterations in cell function. These studies are being performed in collaboration with Dr. Jeffrey Molkentin at the University of Cincinnati. The second and third areas of new research are centered on the new idea that there is myocyte turnover in the adult heart. Therefore, we are studying the factors that regulate cell death and new myocyte formation. We have identified cardiac stem/progenitor cells in feline and human hearts and plan for a rapid expansion of this novel (and controversial) area. We will specifically explore the hypothesis that hypertrophy in response to pressure overload involves new myocyte formation in addition to enlargement of terminally differentiated myocytes.
We have recently identified a novel stem cell that resides within cortical bone. These cortical bonce derived stem cells (CBSCs) have the ability to improve cardiac structure and function when they are injected into the heart after myocardial infarction. The potential clinical utility of these cells is being studies in a preclinical model of ischemic heart disease. We are also examining the exosomes derived from CBSCs harbor factors that are responsible for their cardioprotective features.