In This Section

Steven R. Houser, PhD, FAHA

Senior Associate Dean, Research
Vera J. Goodfriend Endowed Chair, Cardiovascular Research
Chair and Professor, Physiology
Director, Cardiovascular Research Center (CVRC)
Professor, Medicine

Steven Houser
For Patients
Contact Information

Contact Information

Phone

215-707-3278

Fax

215-707-0170

Email

srhouser@temple.edu

Office

MERB 1041
About Me

Research Interests

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) regulate 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 (mainly through apoptosis, with Dr. Richard Kitsis) and new myocyte formation (via cardiac progenitor cells, with Drs Annarosa Leri and Piero Anversa). 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. Our newest data shows that expression of T-type Ca2+ channels is linked to differentiation of cardiac stem cells into new cardiac myocytes. Ca2+ influx through these channels also appears to be linked to proliferation of new myocytes.

Education, Training & Credentials

Educational Background

  • Postdoctoral Fellowship, Cardiology, Lewis Katz School of Medicine at Temple University
  • PhD, Physiology, Lewis Katz School of Medicine at Temple University
  • BA, Biology and Chemistry, Eastern College
Publications

PubMed Publications

View PubMed Publications