Department of Pharmacology
Basic Science Building, Rm. 501
15 Dana Road
Valhalla, NY 10595
Our research is focused on two major areas: 1) the regulation of coronary collateral growth, and 2) the mechanisms by which 20-HETE antagonists minimize myocardial infarct size and prevent left ventricular dysfunction after myocardial infarction.
Regulation of coronary collateral growth
Coronary collateral growth (CCG), an adaptive process to transient, repetitive myocardial ischemia characteristic of stable angina pectoris is severely compromised in metabolic syndrome resulting in greater incidence and severity of myocardial infarctions and higher mortality in this patient population. The aim of our studies is to elucidate signaling pathways and cellular processes which are necessary and sufficient for coronary collateral formation in normal, healthy animals, and determine how they are altered in metabolic syndrome in order to develop treatment paradigms to restore CCG in metabolic syndrome. Current work focuses on how restoration of normal 20-HETE and miR-145 levels leads to complete restoration of CCG and controls critical regulatory aspects of CCG including ECM modulation, endothelial function and inflammation.
Beneficial mechanisms of 20-HETE antagonists
Recently, we have found that 20-HETE levels were significantly elevated during myocardial infarction (MI) in animal models and humans. Our 20-HETE antagonists minimized myocardial infarct (MI) size, as well as left ventricular dysfunction and mortality in both normal and metabolic syndrome animals. Current and future work will focus on exploring the mechanism which underlay this effect in animals models and in human patients, as well on developing a treatment paradigm to achieve maximal infarct size reduction and delay or prevent development of post-MI heart failure.