Primary Mentors

Glenn I. Fishman, MD
Medicine (Cardiology) – Program Director, Primary Mentor

Dr. Fishman's laboratory focuses on several aspects of cardiovascular biology and disease, including: gap junction channels and the regulation of cardiac impulse propagation; cardiac conduction system development and disease; cardiac stem cell biology; and ischemia-reperfusion injury. The laboratory utilizes a multi-disciplinary approach including molecular and cellular biology, transcriptional profiling, cellular, organ-level and in vivo electrophysiology, as well creation and characterization of novel genetically engineered murine models. The Fishman laboratory is supported by grants from the NIH and NYSTEM. Dr. Fishman currently serves as chair of the NIH Electrophysiology, Signaling, Transport and Arrhythmias (ESTA) Study Section; is a member of the AHA Scientific Sessions Program Committee; and chair of the Basic Science Committee of the Heart Rhythm Society.

Leon Axel, MD, PhD
Radiology – Primary Mentor

Dr. Axel’s laboratory is interested in developing and using imaging approaches, particularly involving MRI, for the quantitative evaluation of cardiovascular structure and function in health and disease. A major focus of the laboratory is developing methods for quantifying regional cardiac function and perfusion. The laboratory utilizes a multi-disciplinary approach, ranging from the development of basic imaging and image analysis methods to their application to patient studies.

Jeffrey Berger, MD
Medicine (Cardiology) - Primary Mentor
Dr. Berger is an Assistant Professor at New York University School of Medicine in the Departments of Medicine and Surgery in the Divisions of Cardiology, Hematology, and Vascular Surgery. Dr. Berger has a particular interest in the field of platelet and hypercoagulable mechanisms of cardiovascular disease, with research interests that include: (1) the role of platelet activity in patients with different high risk vascular phenotypes, such as cardiac and peripheral atherosclerosis, aneurysmal disease, venous disease, kidney disease, and HIV; (2) regulation of platelet activity during the perioperative period; (3) the clinical and platelet response to antiplatelet and antithrombotic therapeutics; and (4) the study of personalized medicine using the platelet phenotype to guide therapeutics. Dr. Berger has set up a platelet lab to measure platelet activity using various techniques, including whole blood and platelet rich plasma aggregometry, flow cytometry, hematology analysis, and molecular biology using the platelet transcriptome. The overall goal of the lab is to use the platelet phenotype in understanding who is at risk for developing cardiovascular disease and to determine whether modification of the platelet phenotype can ultimately lower the risk of adverse cardiovascular events. Dr. Berger is a current recipient of the Doris Duke Charitable Foundation’s Clinical Scientist Development Award for his study on platelet activity in cardiovascular disease, American Heart Association Fellow to Faculty Award to study the relationship between sex, platelet activity and platelet directed therapies, and the Center for AIDS Research Award to study platelet activity, inflammation and the response to antiplatelet therapy in HIV.

William A. Coetzee, PhD
Pediatrics (Pediatric Cardiology) – Primary Mentor

Dr. Coetzee's program is focused on examining electrophysiological processes in the cardiovascular system, with emphasis on K+ channels and their role in regulating cardiac excitability in health and disease. They are currently examining the hypothesis that glycolytic enzymes are integral components of the KATP channel macromolecular complex that regulate KATP channel activity under physiological and pathophysiological conditions. His group is also using exploring the regulation of vascular function by KATP channels. They recently described a novel role for KATP channels to regulate vascular tone via an endothelin-1 dependent mechanism. Finally, they are performing studies to examine the roles of endothelial KATP channels during pathophysiological insults, such as changes in coronary flow during hypoxia and ischemia and the myocardial response and infarct size in response to ischemia/reperfusion.

Bruce Cronstein, MD
Medicine (Clinical Pharm) – Steering Committee, Primary Mentor

Dr. Cronstein studies various aspects of adenosine metabolism and receptors in rheumatologic diseases, wound healing, hepatic fibrosis and vascular disease. One discovery, the use of adenosine A2A receptor agonists for the promotion of wound healing, has been licensed to King Pharmaceuticals, and a lead compound has recently finished Phase II clinical trials for the treatment of diabetic foot ulcers; a Phase III trial is now in the planning stages. Dr. Cronstein’s laboratory has demonstrated that adenosine and its receptors mediate the anti-inflammatory effects of methotrexate, an agent which has particular efficacy in reducing the risk of myocardial infarction and stroke in patients with rheumatoid arthritis. Preliminary studies indicate that adenosine and its receptors on endothelial cells and macrophages mediate this effect by diminishing leukocyte adhesion to vascular endothelium, by diminishing foam cell formation, and by promoting reverse cholesterol transport from the vessel wall to the liver.

Mario Delmar, MD, PhD
Medicine (Cardiology) - Primary Mentor

The mechanisms responsible for ventricular arrhythmias in patients with cardiomyopathies are poorly understood. It is the long-term objective of our laboratory to gain knowledge on how disruption of mechanical function can alter the electrical stability of the heart. Our research focuses on the interactions occurring at the intercalated disc. Specifically, we study the cross-talk between molecules involved in mechanical coupling (desmosomes; adherens junctions) and those involved in the propagation of electrical signals between cells (gap junctions; sodium channels). It is our central hypothesis that rather than independent, these complexes closely interact with one another, so that loss of mechanical integrity can lead to electrical dysfunction and arrhythmias. These studies require a multi-disciplinary approach involving biochemistry, cellular and multicellular electrophysiology, microscopy and molecular biology. Our studies seek translation into the molecular mechanisms responsible for lethal arrhythmias in patients afflicted with arrhythmogenic right ventricular cardiomyopathy (ARVC), an inherited disease associated with sudden death in the young and linked to mutations in proteins of the cardiac desmosome, a structure responsible for mechanical continuity between cardiac cells.

Edward A. Fisher, MD, PhD
Medicine (Cardiology) – Steering Committee, Primary Mentor

Dr. Fisher’s laboratory focuses on the cell biology of hepatic lipid and lipoprotein metabolism and the regression of atherosclerosis. Dr. Fisher’s laboratory was the first to show that this degradation is mediated by the ubiquitin-proteasome pathway and the cytosolic chaperone, Hsp70. His lab has also been the first to demonstrate a non-proteasomal pathway of apoB degradation regulated by dietary fatty acids, a process that may also be regulated by insulin. Importantly, this non-proteasomal pathway may be dysregulated in insulin-resistance (such as seen in patients with type II diabetes or obesity) and, thereby, contribute to the over-production of atherogenic lipoproteins that increase the risk of coronary artery disease in these metabolic states. His laboratory is using cell and molecular biological approaches on experimental models as diverse as cell-free systems and tissue-specific knockout mice. In addition, his laboratory investigates the enzymes in the liver responsible for the esterification and hydrolysis of cholesteryl esters. Dr. Fisher’s laboratory is also interested in the molecular factors that regulate the progression and regression of atherosclerotic plaques, as well as the development of novel plaque imaging agents. This research relies on mouse models of atherosclerosis and current projects focus on: the regression of plaques after the normalization of hyperlipidemia; the effects of HDL on plaque progression and regression; the lipid-independent role of apoE on neointima formation after arterial injury; the effects of hyperglycemia and insulin-resistance as separate factors on atherosclerosis progression and regression; and the mechanisms by which HDL can deliver imaging agents to plaques for their non-invasive assessment.

Michael Garabedian, PhD
Microbiology – Primary Mentor

Dr. Garabedian studies gene regulation by nuclear hormone receptors, including LXRa, which is a key regulator of cholesterol homeostasis in macrophages. Dr. Garabedian's lab has collaborated extensively with Dr. Fisher on the mechanism of regulation of CCR7 by LXRa in macrophages during regression of atherosclerosis. In particular his group has been examining the role of LXRa phosphorylation in gene regulation in macrophages. He has found that the expression of the chemokine receptor CCR7, which promotes macrophage emigration from atherosclerotic lesions in a mouse model of atherosclerotic plaque regression, was over 15-fold higher in macrophages expressing a phosphorylation deficient LXR alpha mutant compared to macrophages expressing the wild-type phosphorylated form of LXR alpha. His group is currently examining the mechanism of LXRa phosphorylation dependent regulation of CCR7 gene expression. They are also screening for novel LXR ligands that activate CCR7 expression in macrophages by mimicking the non-phosphorylatable LXRa conformation. Such a ligand could represent a potential new class of therapeutics that facilitate atherosclerotic plaque regression and decrease heart failure.

Judith S. Hochman, MD
Medicine (Cardiology), Program Co-Director, Primary Mentor

Judith S. Hochman, M.D., is the Senior Associate Dean for Clinical Sciences, Co-Director of the NYU-HHC Clinical and Translational Science Institute, Harold Snyder Family Professor and Associate Director of the Leon Charney Division of Cardiology and Director of the Cardiovascular Clinical Research Center at NYU Langone Medical Center.

Dr. Hochman holds a Masters Degree in Cellular and Developmental Biology from Harvard University and an M.D. from Harvard Medical School. She completed Internal Medicine training at the Peter Bent Brigham Hospital and Fellowship in Cardiovascular Medicine at the Johns Hopkins University Medical Center. She currently serves on the National Heart Lung and Blood Institute (NHLBI) Board of External Experts and the Science Advisory Coordinating Committee of the American Heart Association, on the FDA/CDER Cardiovascular and Renal Drugs Advisory Committee, the American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines, and the AHA National Research Committee. She has authored over 250 publications and chapters in major internal medicine and cardiovascular textbooks. She is a Senior Guest Editor for Circulation and serves on editorial boards of European Heart Journal and American Heart Journal.

She has led, as Study Chair, NHLBI funded international randomized clinical trials that tested the optimal management for subsets of patients with ischemic heart disease. These studies led to two new recommendations regarding the role of revascularization (stents and coronary bypass surgery) in the ACC/AHA Practice Guidelines. Dr. Hochman is currently leading an NHLBI funded comparative effectiveness ISCHEMIA trial in over 300 sites in 33 countries worldwide comparing a routine invasive strategy (cardiac catheterization with stents or coronary bypass surgery) and an initial conservative strategy in patients with stable ischemic heart disease and at least moderate ischemia. She was also the Study Chair for the first phase 2 and phase 3 multicenter randomized trials conducted to test a pharmacologic agent, a nitric oxide synthase inhibitor, for cardiogenic shock (SHOCK 2 and TRIUMPH). She has also served on numerous Data Safety Monitoring Boards and Steering Committees of international clinical trials investigating the role of novel agents in acute coronary syndromes and stable ischemic heart disease.

Dr. Hochman has also served as a mentor for numerous trainees who have gone on to have successful independent careers. In 2008 she received the American Heart Association Women in Cardiology Mentoring Award. She is a 2014 Awardee of the AHA Clinical Research Prize.

Stuart Katz, MD
Medicine (Cardiology) – Steering Committee, Primary Mentor

The major scientific focus of the Katz laboratory is patient-oriented research in human physiology and pharmacology. Numerous techniques for assessment of vascular physiology and nitric oxide metabolism have been developed in the laboratory to explore the role causes and consequences of vascular dysregulation in heart failure and other disease states. In addition to ongoing investigations in heart failure populations, Dr. Katz is pursuing clinical investigations on the role of iron metabolism in pathogenesis of atherosclerosis, and the cytoprotective role of erythropoietin in acute coronary syndromes. The panel of non-invasive techniques for assessment of vascular physiology developed in the laboratory (high-resolution vascular ultrasound, venous occlusion plethysmography, arterial pulse contour and pulse velocity analysis, exhaled nitric oxide production, stable isotopes for assessment of nitric oxide metabolism) has also led to collaborations with other patient-oriented investigators with backgrounds in psychiatry, obstretrics and gynecology, environmental medicine, occupational medicine, pediatric and adult endocrinology, and sleep medicine, and translational collaborations with basic investigators in vascular biology. In addition to his extensive experience in the conduct of patient-oriented research, Dr. Katz holds a K24 midcareer award in patient-oriented research and has a strong track record in mentoring young investigators with a diverse array of educational and ethnic backgrounds.

Kathryn Moore, PhD
Medicine (Cardiology) – Primary Mentor

Kathryn Moore is an Associate Professor at New York University School of Medicine in the Marc and Ruti Bell Vascular Biology and Disease Program. Dr. Moore is an established researcher in the field of inflammatory mechanisms of atherosclerosis, with research interests that include: (1) molecular mechanisms of sterile inflammation in atherosclerosis and Alzheimer’s disease, (2) regulation of cholesterol metabolism, and (3) role of positive and negative guidance cues in leukocyte trafficking. Using a variety of biochemical, genetic, cell and molecular biology techniques, Dr. Moore’s laboratory has uncovered novel roles for scavenger receptor, nuclear hormone receptor and Toll-like receptor pathways in the host response to infection and modified-self ligands that accumulate in disease states. Her research has improved our understanding of how immune cells respond to atherogenic lipids and b-amyloid, and contribute to the pathology that underlies sterile inflammatory diseases such as atherosclerosis and Alzheimer’s disease. Dr. Moore’s research aims to further the understanding and prevention of chronic inflammatory disorders through interdisciplinary study of the molecular mechanisms regulating the initiation, promotion and resolution of macrophage inflammatory responses. This work has received extramural funding from the National Institutes of Health, Ellison Medical Foundation, American Heart Association and American Health Assistance Foundation. Most recently, Dr. Moore was awarded a Challenge Grant from the NIH for her work on novel guidance cues regulating leukocyte trafficking and inflammation.

Dr. Moore has been the recipient of numerous awards, including the Claflin Distinguished Scholar Award, the Ellison New Scholar in Aging Award and the American Heart Association’s Special Recognition Award in Vascular Biology. Dr. Moore serves on the editorial board of the Arteriosclerosis, Thrombosis and Vascular Biology journal and is a member of the American Heart Association’s Leadership Committee for Arteriosclerosis, Thrombosis and Vascular Biology, which provides input into the AHA’s science positions and recommendations for needed activities in the area of medicine and research in cardiovascular disease.

Gregory E. Morley, PhD
Medicine (Cardiology) – Primary Mentor

Dr. Morley's current research interests focus on determining the molecular mechanisms responsible for cardiac arrhythmias. One major area of interest includes studies determining the arrhythmogenic role of dysregulation of cardiac gap junctions. A second area of interest involves determining the mechanisms that are responsible for the developmental changes in impulse initiation and conduction within the sinus node and atria. Dr. Morley is one of the world’s experts in the use of high-speed imaging techniques to study electrical wave propagation at both the macroscopic and cellular level. He has developed novel quantitative methods to accurately define and measure patterns of wave propagation, conduction velocity and wave front curvature on the epicardial and endocardial surfaces of adult, newborn and embryonic mouse hearts. With this technology, His group uses this technology to characterize normal and abnormal conduction patterns and has obtained the first high-resolution images of electrical wave propagation in mice lacking various cardiac gap junction proteins.

Evgeny Nudler, PhD
Biochemistry – Primary Mentor

Dr. Nudler's original work on transcription explained how RNA polymerase moves and recognizes pausing and termination signals in DNA and RNA. His studies on bacterial gene regulation led to the discovery of riboswitches (metabolite-sensing RNA) that control numerous bacterial genes. More recently, his group uncovered key regulators of the heat shock response in eukaryotic cells. Dr. Nudler has also made important contributions in the area of nitric oxide biochemistry in both animal and bacterial systems. This recent line of investigation has led to novel therapeutic strategies to modulate nitric oxide abundanc and bioreactivity, and influence cardiovascular hemodynamics as well as reperfusion injury.

Gbenga Ogedegbe, MD
Medicine (General Internal Medicine) – Primary Mentor

The programmatic focus of his research is the translation into primary care practices, and dissemination of evidence-based behavioral interventions targeted at cardiovascular risk reduction in minority and underserved populations. He has extensive experience in the development and implementation of practice-based clinical trials of behavioral interventions targeted at blood pressure control in African Americans. He is the PI of an NIH-funded R01 trial, a Project Leader on an NCMHHD-funded P60 Health Disparities Center for Health of Urban Minorities, and a Co-Investigator on several NIH-funded trials designed to improve medication adherence and blood pressure control in minority patients. He has completed several studies that examined the barriers faced by this population regarding expectations of blood pressure management, medication adherence, and most recently successfully tested the effectiveness of motivational interviewing counseling in improving medication adherence and blood pressure control in African-Americans.

Charles S. Peskin, PhD
Mathematical Sciences – Primary Mentor

Dr. Peskin's principal research effort is to create a mathematical/computer model of the heart. The key methodology of this effort is the immersed boundary (IB) method, which Peskin introduced for the computer simulation of flow patterns around heart valves and the computer-assisted design of prosthetic cardiac valves. A whole-heart simulator, based on the IB method, has since been developed by Drs. David McQueen and Peskin. The computer program that implements this Virtual Heart solves the fluid-structure interaction problem of blood flow in the cardiac chambers coupled to the active contractility of the muscular heart walls and the passive elasticity of the flexible heart valve leaflets. Dr. Peskin (with Drs. Boyce Griffith, NYU Department of Medicine, and Edward Vigmond, University of Calgary) is also modeling the electrophysiology of the heart along with cardiac mechanics, with the same muscular fiber architecture used as the foundation for both computations. This has been achieved in a computational study on the effect of bundle branch block on cardiac output. A novel computational method for the bidomain equations of cardiac electrophysiology has been developed by Drs. Griffith and Peskin, and has been tested successfully in idealized geometries that include fiber rotation. This methodology adapts the concepts and data structures of the IB method from the domain of cardiac mechanics to that of cardiac electrophysiology, thus laying the groundwork for the study of electromechanical interaction and the computational optimization of cardiac resynchronization therapy.

Silvia G. Priori, MD, PhD
Medicine (Cardiology) – Primary Mentor

Dr. Priori has established a vibrant translational and clinical research program in cardiovascular genetics, with a particular focus on inherited channelopathies and other inherited forms of heart disease. Beginning almost two decades ago, Dr. Priori established a clinical database of patients with known or suspected inherited arrhythmias, including long QT syndrome, Brudaga syndrome, catecholaminergic polymorphic VT, ARVC, short QT syndrome and related disorders. Her work defined the genetic basis for CPVT and her clinical database analyses have facilitated genotype-phenotype studies that have been of substantial clinical importance. Dr. Priori’s most recent work focuses on establishing murine models of the various human inherited channelopathies, with the goal of developing targeted gene and/or pharmacologic therapies for these disorders. Dr. Priori has been well-funded by a variety of European funding agencies, including TELETHON, the Italian Health Ministry and the LEDUCQ Foundation, and in the past she has served as an investigator on grants from the NIH.

Daniel Rifkin, MD
Cell Biology – Primary Mentor

The Rifkin laboratory is focused on several themes that relate to the fundamental biology of TGF-ß and its activation. They are elucidating the mechanisms that convert latent to active TGF-ß and have described activation by proteases and by the integrin avß6, as well as by sheer in the vascular system. His laboratory is also examining the interactions of LTBPs with ECM components with the ultimate goal of understanding latent TGF-ß activation in a way that will permit the design of inhibitors for specific activation pathways. His laboratory is also studying LTBP function by creating mouse mutants in which either null mutations have been introduced into the LTBP genes, or point mutations in LAP have been generated that will block the TGF-ß propeptide from binding to LTBP. These mutations have revealed several interesting phenotypes in bone, heart, lung and fat differentiation and are informative with respect to aspects of TGF-ß biology. Third, his laboratory is interested in the role of TGF-ß in Marfan syndrome (MFS). They have shown that in MFS the vascular smooth muscle cells (VSMCs) activate latent TGF-ß whereas the normal VSMCs do not and proposed a model to explain the molecular pathogenesis in this syndrome. This model has been tested in mice and man using administration of an AT1 antagonist, where it has been shown to decrease the progression of the manifestations of MFS.