Washington University School of Medicine - Cardiovascular Division - Center for Cardiovascular Research

  

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Anthony J. Muslin, M.D. - My research is focused on the molecular causes of cardiac hypertrophy and congestive heart failure. We use transgenic and "knockout" mouse systems to examine the molecular mechanisms of growth factor action. I am particularly interested in mitogen-activated protein (MAP) kinase cascades.

Dana R. Abendschein, Ph.D. - Our research in this physiology laboratory focuses on the molecular responses of the arterial wall and heart to injury.

Nada A. Abumrad, Ph.D. - The research of Dr Abumrad’s group deals with the molecular mechanisms regulating utilization of fatty acids, an important component of the western diet. She identified the plasma membrane protein CD36 as a facilitator of cellular FA uptake and is now examining how CD36 level modulates the acute and chronic responses of muscle and adipose cells to energy fluctuations and other stresses. A major focus in the intact animal is on the metabolic impact of dysregulated FA utilization by studying mice models of tissue-specific variations in CD36 gene level. The long term goal is to translate the findings in rodents to humans where polymorphisms in the CD36 gene are common. Humans with CD36 deficiency have impaired myocardial FA uptake, abnormalities of plasma lipids and a higher risk of diabetes-associated heart disease.

George Broze, Jr., M.D. - The goal of our research is an understanding of the initiation and control of hemostasis and the interrelationship between coagulation and inflammation. Rather than hemorrhagic phenomena, the investigative thrust concerns pathologic thrombosis and atherosclerosis.

Peter A. Crawford, M.D., Ph.D. - We employ systems biology approaches to decipher the relationship between nutrient biotransformation-absorption (including the host-microbial interface) and integrated energetic homeostasis. A particular focus is to use the myocardium as a reporter of substrate delivery and utilization in genetic and environmental backgrounds that will help us gain greater understanding of metabolic (mal)adaptation to states of nutrient deficiency or excess.

Sharon Cresci, M.D. - My research focuses on genetic and pharmacogenetic associations with diabetic cardiovascular disease, with a particular interest in PPAR-pathway genes.

Gerald W. Dorn, II, M.D. - The Dorn Lab studies many factors relating to how the heart adapts to increased stress, and how these adaptive mechanisms ultimately fail. Our primary area of interest concerns the multiple biochemical signaling pathways for growth and death of heart cells that are activated through the actions of circulating and local neurohormones (such as angiotensin II, epinephrine and norepinephrine, and endothelin-1) on their G-protein-coupled cardiac myocyte membrane receptors.

Brian N. Finck, Ph.D. - The overall objective of my lab is to characterize abnormalities in cardiac, hepatic, and skeletal muscle metabolism in obesity and type 2 diabetes with particular focus on the molecular mechanisms involved in these metabolic changes. To accomplish this, we employ a variety of approaches including molecular biological techniques, genomic expression profiling, cell culture-based systems, and transgenic mouse models.

William A. Frazier, Ph.D. - We are using knockout mice to investigate the role of thrombospondins and their receptors CD36 and CD47 in the response of the vessel wall to injury (neointimal hyperplasia) and in autoimmunity and inflammatory responses contributing to atherogenesis and plaque instability.

Richard W. Gross, M.D., Ph.D. - We study the regulation of reactions which generate lipid second messengers derived from membrane phospholipids and the effects of alterations in membrane organization, membrane-protein interactions and membrane dynamics on these processes.

Patrick Y. Jay, M.D., Ph.D. - Heterozygous mutations of the cardiac transcription factor Nkx2-5 cause congenital cardiac malformations and atrioventricular block in man. My laboratory studies the mechanisms involved in the pathogenesis of these defects and in the function of Nkx2-5 in the postnatal heart, using a combined developmental, molecular, genetic and physiologic approach. In addition, we are working to elucidate the transcriptional logic of Nkx2-5 target genes and of gene expression in heart failure via experimental and computational methods.

Daniel P. Kelly, M.D. - We are interested in the molecular regulatory mechanisms involved in the control of mitochondrial energy production during cardiac development, and in the hypertrophied, failing, diabetic, and ischemic heart. A second focus involves the investigation of the role of perturbations in cardiac myocyte lipid metabolism in the pathogenesis of inherited and acquired forms of heart failure.

Attilla Kovacs, M.D. - The overall objective of the research is the development and validation of noninvasive ultrasound­based techniques, including quantitative ultrasonic tissue characterization, in small animal models of cardiomyopathies to determine the specific underlying mechanisms responsible for the altered backscatter characteristics of the myocardium in a variety of cardiac diseases.

Sándor J. Kovács, Jr., Ph.D., M.D. - Areas of interest include: Characterization of physical properties of cardiovascular tissue; maximal information extraction from in-vivo physiologic signals; mathematical modeling of cardiovascular function; nonlinear dynamics and thermodynamics of cardiovascular function; and development of new technology for imaging and physiologic signal processing. Click here for Cardiovascular Biophysics Laboratory website.

Gregory M. Lanza, M.D., Ph.D. - Our primary research interests are focused upon noninvasive molecular imaging and drug delivery research, i.e., tissue specific imaging and therapy.

John J. Lehman, M.D. - We are interested in understanding fundamental mechanisms of age-associated disease, including the decline in cardiac systolic and diastolic function with age. Additionally, we are investigating the role of altered transcriptional regulation of mitochondrial function in facilitating the benefits of age-retarding interventions such as calorie restriction.

Robert P. Mecham, Ph.D. - The major goal of our research is to understand the complex process of extracellular matrix secretion and assembly, with a particular focus on elastic fibers and how extracellular matrix influences the phenotype of cells. We have a longstanding interest in understanding the development of the pulmonary circulation and vascular changes that occur in pulmonary hypertension.

James G. Miller, Ph.D. - The focus of our research is on the anisotropic elastic and viscoelastic properties of cardiovascular tissue. We explore methods for the characterization of myocardium and for improving echocardiographic imaging that make use of the physics underlying the interaction of ultrasonic waves with anisotropic tissue.

Anthony J. Muslin, M.D. - My research is focused on the molecular causes of cardiac hypertrophy and congestive heart failure. We use transgenic and "knockout" mouse systems to examine the molecular mechanisms of growth factor action. I am particularly interested in mitogen-activated protein (MAP) kinase cascades.

Jeanne Nerbonne, Ph.D. - Research in our laboratory is focused on delineating the mechanisms involved in the regulation and modulation of voltage-gated ion channels in cardiac myocytes and cortical neurons.

Daniel S. Ory, M.D. - Work in my laboratory focuses on identification and characterization of genes that function in the uptake, intracellular transport, and export of lipoprotein-derived cholesterol.

Yoram Rudy, Ph.D. - Our research aims at understanding the mechanisms that underlie normal and abnormal rhythms of the heart at various levels, from the molecular (ion channel) and cellular to the whole heart. We are also developing a novel noninvasive imaging modality (Electrocardiographic Imaging, ECGI) for the diagnosis and guided therapy of cardiac arrhythmias. Through the development of detailed mathematical models of cardiac cells and tissue, we are investigating the mechanisms and consequences of genetically-inherited cardiac arrhythmias, impaired cell-to-cell communication, and abnormal spread of the cardiac impulse in the diseased heart (e.g. myocardial infarction). ECGI imaging is currently being tested and evaluated in patients with various heart conditions. See http://rudylab.wustl.edu and http://cbac.wustl.edu.

Nandakumar Sambandam, Ph.D. - My research focuses on metabolic alterations that the heart undergo during various physiological and pathological conditions and identifying metabolic targets which can be used as therapeutic approaches to treat cardiovascular diseases.

Jean E. Schaffer, M.D. - The goals of studies in the Schaffer lab are to characterize the fundamental cellular mechanisms of lipotoxicity, and to understand how these processes contribute to organ dysfunction in rodent models of metabolic disease.

Clay Semenkovich, M.D. - Our work is focused on lipid metabolism and how it promotes atherosclerosis in the setting of diabetes.

Dwight A. Towler, M.D., Ph.D. - Our group is interested in the mechanism vascular calcification, a process that mechanistically overlaps that of bone formation. Using in vivo and in vitro models, we study how metabolic signals control the osteogenic differentiation of vascular mesenchymal progenitors, programmed by paracrine BMP and Wnt/Dkk1 signaling.

Samuel A. Wickline, M.D. - Our investigative work has focused on the use of ultrasonic tissue characterization for delineation of physiologic and pathologic structure and function of heart and vascular tissues.

Kathryn A. Yamada, Ph.D. - Research interests include cellular electrophysiologic mechanisms that lead to ventricular arrhythmias and sudden cardiac death during myocardial ischemia, infarction, hypertrophy, and failure.

 

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Center for Cardiovascular Research
Department of Medicine
Washington University School of Medicine