Trainees
Current Trainees
Luigi Adamo, MD, PhD
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Joshua Brettmann, PhD
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Michael Cooper, PhD
Michael is examining the role of acetylation and deacetylation of lipin 1 by HDAC1, a protein known to be activated in failing heart. Preliminary work suggests that maintaining lipin 1 expression in the hearts of animals undergoing transaortic constriction preserves cardiac function. Future works will examine the effects of over expressing acetylation deficient lipin 1 to examine the effect on cardiac metabolism and the response to pathological stimuli.
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McKenna Feltes, PhD Candidate
DBBS Pre-Doc Trainee, Washington University School of Medicine
Exogenous cholesterol is acquired principally through receptor-mediated endocytosis of cholesteryl ester-laden low-density lipoproteins and trafficked to the lysosome where it is distributed to other cellular organelles. While it is well established that bulk export of lysosomal cholesterol is dependent on lysosomal protein NPC1, NPC1- dependent and lower flux, NPC1-independent post-lysosomal cholesterol trafficking pathways are poorly understood. My work aims to identify the proteins involved in this trafficking using novel cholesterol probes. Recent Publications: |
Jesus Jimenez, MD, PhD
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Billy Kang, MD, PhD Candidate
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Andrew Koenig, PhD
My project focuses on using zebrafish to define the mechanisms by which identified human gene variants associated with dilated cardiomyopathy result in heart failure. Additionally, I am utilizing murine models to investigate the role of macrophage heterogeneity in response to acute myocardial injury.
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Chien-Jung Lin, MD, PhD
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Kathryn Mangold, PhD Candidate
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Jonathan Moreno, MD PhD
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Arthur Sletten, MD, PhD Candidate
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Kir2.1 is crucial for setting the resting membrane potential and misregulation of this channel have significant impact on the timing of cardiac action potentials, with mutations leading to both long and short QT syndromes. My project looks to understand the molecular mechanism of this crucial channel by using single molecule FRET to determine the structural and dynamic consequences of lipid binding.
The Notch signaling pathway is a key player in early cardiovascular development that becomes quiescent in the healthy adult heart. During periods of stress, such as myocardial infarction, Notch can be reactivated in adults to promote cardiomyocyte survival, enhance progenitor proliferation, promote angiogenesis and reduce fibrosis. In addition, Notch reactivation can induce cardiac electrical remodeling, which may alter the electrical properties of the heart and result in a pro-arrhythmic state that increases the risk for sudden cardiac death. The primary goal of my project is to elucidate the role of Notch signaling with regards to cardiac electrical remodeling in the setting of cardiac injury.
I am studying the structure and function of the voltage-gated potassium channel KCNQ1. KCNQ1 is a critical ion channel in the heart and plays an important role in the heart’s ability to respond to stress. Utilizing electrophysiological and optical techniques, I’m trying to learn about how KCNQ1 works on the molecular level and how dysfunction in KCNQ1 can lead to human disease.
My work focuses on the role of extracellular matrix on the development and remodeling of blood vessels.
My research focus is on utilizing computational approaches to mathematically describe the biology of ion channels, which are critically important for cellular excitability. These models allow us to design better treatment strategies for the pharmacological management of heart failure and arrhythmia. Using computational tools and clinical datasets, I also am interested in drug-repositioning – using old drugs for new targets in novel ways. My current project is focused on building a computational model of the cardiac Na+ channel that incorporates voltage clamp fluorometry data (VCF) to track voltage-sensing domain (VSD) movement of the Na+ channel during an action potential. By incorporating VSD kinetics into a multi-scale model of the heartbeat, we can better understand the molecular movements that drive antiarrhythmic efficacy (or failure) of certain long-QT mutation carriers in response to commonly prescribed anti arrhythmic drugs.
Excess lipid uptake and metabolism cause cell dysfunction and death in a process called lipotoxicity. Our laboratory has identified several novel genes that regulate lipotoxicity, and my project focuses on one of these genes, the small nucleolar hosting gene 3 (snhg3). Disruption of snhg3 protects cells from lipotoxic cell death through rewiring of glucose metabolism. Ongoing work seeks to identify the molecular underpinnings of this phenotype and investigate the role of the snhg3 locus in models of in vivo lipotoxicity.
Former Trainees
Peter Crawford, MD, PhD
Professor, Departments of Medicine, and Biochemistry, Molecular Biology, and Biophysics
Our group performs studies in animal models and humans to learn how alterations of ketone metabolism and related pathways may serve as diagnostic biomarkers and therapeutic targets for obesity, diabetes, nonalcoholic fatty liver disease (NAFLD/NASH), and heart failure. We leverage recent advances in stable isotope tracer based NMR and mass spectrometry-based untargeted metabolomics technologies to study metabolism on a systems level, and we also employ established techniques in molecular cell biology and biochemistry to reveal phenotypic shifts at the cellular level. Recent Publication: |
Sharon Cresci, MD
Associate Professor of Medicine (Tenured) and Associate Professor of Genetics, Washington University School of Medicine
The focus of my research is the association of genetic variation with clinical outcomes in patients with cardiovascular disease and in the variable response to pharmacologic treatment. I have specific interest in (1) the contribution of genetic variation to racial disparities in response to medical treatments used to treat coronary syndromes and in outcomes in patients with coronary artery disease and (2) defining the functional mechanism of these genetic associations; the ultimate goal of my research is to promote and advance precision medicine approaches. Recent Publication: |
Slava Epelman, MD, PhD
Assistant Professor of Medicine
We study cardiac immune cell heterogeneity and the role of individual immune cell subsets in cardiac tissue injury, repair and regeneration. Recent Publication: |
Brian Finck, PhD
Associate Professor in Medicine, Washington University School of Medicine
The Finck lab studies basic aspects of intermediary metabolism in heart, skeletal muscle, and liver. We have ongoing projects to study the role of key proteins that control lipid synthesis and mitochondrial metabolism of fatty acids and pyruvate.
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Christopher Holley, MD, PhD
Assistant Professor of Medicine, Duke University
The goal of my laboratory at Duke University is to understand how emerging aspects of RNA biology contribute to cardiovascular health and disease, then translate those findings into novel therapeutic approaches for patients. Right now, I am particularly interested in studying how non-coding RNAs and RNA modifications play a role in heart failure. Recent Publication: |
David Lanfear, MD
Head, Advanced Heart Failure and Transplant Cardiology, Professor of Medicine, Henry Ford Hospital
Research focus is genomics and precision medicine for heart failure, HF clinical trials, and the care of the adv. Hf patients (LVAD outcomes, pt selection, etc.).
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Kory Lavine, MD, PhD
Assistant Professor, Washington University School of Medicine
The primary goal of our laboratory is to identify new approaches to treat patients with heart failure. Specific projects in the laboratory are focused on unraveling the mechanisms that initiate disease pathogenesis using a precision medicine approach and defining the role of the immune system in cardiac tissue homeostasis, heart failure progression, and myocardial tissue repair. Recent Publication: |
Babak Razani, MD, PhD
Assistant Professor of Medicine -and- Pathology/Immunology
Babak Razani’s research broadly focuses on the mechanisms of atherosclerosis and related Recent Publication: |
Michael Sack, MD, PhD
Chief, Cardiovascular Branch, Division of Intramural Research NHLBI and Director of Laboratory of Mitochondrial Biology and Metabolism
Studying the role of nutrient sensing and acetylation in the control of mitochondrial biology and metabolism. My laboratory has extended this work into the translational space exploring these concepts in the control of immune function and inflammation.
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Joel Schilling, MD, PhD
Assistant Professor of Medicine, Pathology & Immunology
My lab is focused on understanding the effects of obesity and diabetes on macrophage function. Our goal is to dissect the biology of distinct macrophage populations in vivo to design novel approaches to treat complications of metabolic disease.
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