Physician Directory
Short Bio

Steven O Marx

Name and Degree:
Steven O Marx, M.D.
Associate Professor of Medicine
Background Information

Education and Training

 1982-1986 , Biology, Union College

Medical School:

 1984-1988 , Medicine, Albany Medical College


 1989-1990 , Internal Medicine, University of Rochester-Strong Memorial Hospital


 1990-1992 , Internal Medicine, University of Rochester-Strong Memorial Hospital


 1992-1996 , Cardiology-Clinical Cardiac Electrophysiology, Mount Sinai Medical Center

Board Certification: Internal Medicine
Clinical Cardiac Electrophysiology
Clinical Interests:
Research Interests:
The major goals Dr. Marx's research is to use molecular biological and electrophysiological techniques to develop novel therapies to treat cardiovascular diseases. The high incidence of cardiovascular diseases represents a significant medical problem in the USA and throughout the world, despite remarkable advances over the past few decades. Greater understanding of the molecular mechanisms leading to these disorders will have important implications in improving therapeutic modalities. The research program in cardiovascular diseases has been focused in two major areas: (1) cardiac: studying the regulation of ion channels in normal and pathological conditions in the heart. Altered cardiac ion channel function is associated with heart failure and arrhythmias. (2) vasculature: understanding molecular mechanisms leading to vascular smooth muscle proliferation, migration and contractility. Increased smooth muscle proliferation and migration leads to re-closing of an artery after balloon angioplasty and stent implantation. Increased smooth muscle contractility is associated with hypertension. Each program has led to significant advances in the field.

The ion channel is an integrator of multiple inputs, shaping the cellular/organ response to various hormonal stimuli in normal and diseased states. My ion channel research program is currently focused on two ion channels: the large conductance, Ca2+ activated potassium (K+) channel (BK channel), and the voltage gated cardiac L-type Ca2+ channel (Cav1.2).

From the 1990ís to early 2000ís, restenosis after balloon angioplasty and/or stent implantation occurred with an incidence of approximately 30%, leading to a significant limitation in its effectiveness. Rapamycin (sirolimus) was originally noted to have anti-fungal properties and subsequently, its potent immunosuppressant properties were appreciated. Largely because rapamycin was viewed as an immunosuppressant drug, its potential application for other therapeutic targets remained unappreciated for more than a decade. In the 1990ís, we identified rapamycinís potential utility as an anti-restenosis agent in a series of papers describing its anti-proliferative and anti-migratory properties in vitro and in vivo. The identification and elucidation of the molecular mechanisms underlying rapamycinís effects on vascular smooth muscle cells (VSMC) and a study demonstrating that systemic administration could inhibit restenosis in a porcine balloon angioplasty model led to the development of a rapamycin-coated stent (Cypher) and significantly reduced restenosis in several major USA and foreign studies. We have sought to determine the molecular mechanisms mediating rapamycin sensitivity through the development of rapamycin-resistant myogenic cells and the use of genetically altered mice.


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