Northwestern University Feinberg School of Medicine
Feinberg Cardiovascular Research Institute


Following are descriptions of the lab work done by center members, listed by principal investigator.

Please note that not all work done within these individual labs falls within the goals of the Center for Molecular Cardiology.

 Hossein Ardehali Lab

Role of mitochondria and metabolic processes in cancer growth, cardiac disease and metabolic disorders

Research Description

Our lab focuses on three major areas of research:

Role of proteins involved in cellular and systemic metabolism

TTP is a protein that binds to AU-rich regions in the 3’ UTR of mRNA molecules and causes their degradation.  It has been studied extensively in the field of inflammation, and we recently showed that it also plays a role in cellular iron conservation.  We have also shown that TTP is a key mediator of cellular metabolic processes.  Our studies have demonstrated that TTP regulates glucose, fatty acid and branched-chain amino acid metabolism in the liver and muscle tissue. We also have evidence that TTP directly regulates mitochondrial electron transport chain (ETC) by targeting specific proteins in the ETC complexes. Finally, recent studies demonstrated that TTP also regulates systemic metabolism by targeting FGF-21 expression.  We have both TTP Floxed mice (for the generation of tissue specific TTP knockout mice), and TTP knockout mice in the background of TNF-alpha receptor 1/2 knockout mice (to reduce the inflammatory burden).  Current studies include: 1) role of TTP in liver metabolism of fatty acids and glucose, 2) effects of TTP on mitochondrial proteins, 3) mechanism of TTP regulation of branched-chain amino acid levels, and 4) role of TTP in cardiac metabolism.

Cardiac regeneration

Adult cardiomyocytes regenerate at a very low rate, but neonatal cardiomyocytes grow and replicate at a high rate. We have identified specific tandem zinc-finger (TZF) proteins that bind to mRNAs to regulate cardiac regeneration and cardiac development. Our studies suggest that these proteins may alter DNA repair in response to damage by regulating p53 and helicases. Current projects include: 1) identifying the mechanism by which TZF proteins regulate p53 and DNA damage, 2) characterization of the role of helicases in cellular proliferation and regeneration, and 3) role of TZF proteins in cardiac development.

Characterization of cellular and mitochondrial iron regulation

Our lab has identified a novel mitochondrial protein, ATP-Binding Cassette-B8 (ABCB8), which plays a role in mitochondrial iron homeostasis and mitochondrial iron export.  Mice with ABCB8 knocked out in the heart develop cardiomyopathy and mitochondrial iron accumulation.  In addition, we have shown that a pathway involving mTOR and tristetraprolin, treatment with doxorubicin (an anticancer drug that also causes cardiomyopathy), and SIRT2 protein also impact cellular and/or mitochondrial iron regulation.  Current studies in this area include: 1) further characterization of ABCB8 in iron homeostasis in other organs and disorders, 2) characterization of the mechanism for iron regulation by SIRT2, 3) identification of the mechanism by which mTOR is regulated by iron, 4) role of iron in viral infection, particularly HIV, 5) characterization of the effects of iron on mitochondrial dynamics, and 6) identification of novel mitochondrial-specific iron chelators.

For more information, see Dr. Ardehali's faculty profile.


See Dr. Ardehali's publications in PubMed.


Dr. Ardehali

 Rishi Arora Lab

Understanding the molecular and signaling pathways involved in atrial fibrillation.

Dr. Arora's research interests center on atrial fibrillation (AF), which is the most common rhythm disorder and is a major cause of stroke and morbidity in an aging population. The therapeutic options currently available for AF are not very effective, in part because of the poor understanding of the underlying mechanisms of this arrhythmia.

The focus of the research in Dr. Arora's laboratory is to:

  1. Study the underlying mechanisms of AF using large animal models of AF. A better understanding of the molecular and signaling pathways involved in AF will allow for the discovery of novel therapeutic targets for this arrhythmia
  2. Discover novel therapeutic strategies to modify critical signaling pathways in AF

Current Projects

Dr. Arora and his research team are currently investigating the autonomic profile of the pulmonary veins and the rest of the left atrium in a canine model, especially as it relates to the genesis of AF. For this research, a variety of sophisticated in-vivoex-vivo and in-vitroelectrophysiologic techniques are employed. These include high-density electrophysiologic mapping in live animals (open-chest, epicardial as well as endocardial mapping), high-resolution optical mapping in Langendorf perfused hearts, and confocal microscopy studies of calcium signaling in isolated cardiac myocytes. Also, a variety of molecular biology and protein-chemistry techniques are used to better understand the molecular substrate that underlies AF.

Recent work from our laboratory on autonomic signaling in the left atrium has contributed significantly to an improved understanding of the autonomic mechanisms of AF. Based on these results, we have begun to use unique cell-penetrating peptides and novel minigenes to inhibit key molecular targets that are critical to autonomic signaling in AF.

In addition, our laboratory is also investigating the mechanisms underlying atrial fibrosis (and the resulting substrate for atrial fibrillation).

For more information, see Dr. Arora's faculty profile.


See Dr. Arora's publications in PubMed.

 Paul Burridge Lab

Investigating the application of human induced pluripotent stem cells to study the pharmacogenomics of chemotherapy off-target toxicity and efficacy

Research Description

The Burridge lab studies the role of the genome in influencing drug responses, known as pharmacogenomics or personalized medicine. Our major model is human induced pluripotent stem cells (hiPSC), generated from patient's blood or skin. We use a combination of next generation sequencing, automation and robotics, high-throughput drug screening, high-content imaging, tissue engineering, electrophysiological and physiological testing to better understand the mechanisms of drug response and action.

Our major effort has been related to patient-specific responses to chemotherapy agents. We ask the question what is the genetic reason why some patients have a minimal side-effects to their cancer treatment, whilst others have encounter highly detrimental side-effects. These side-effects  can include cardiomyopathy (heart failure or arrhythmias), peripheral neuropathy,  or hepatotoxicity (liver failure). It is our aim to add to risk-based screening by functionally validating genetic changes that predispose a patient to a specific drug response.

Recent Findings

  • Human induced pluripotent stem cells predict breast cancer patients’ predilection to doxorubicin-induced cardiotoxicity
  • Chemically defined generation of human cardiomyocytes

Current Projects

  • Modeling the role of the genome in doxorubicin-induced cardiotoxicity using hiPSC
  • Investigating the pharmacogenomics of tyrosine kinase inhibitor cardiotoxicity
  • hiPSC reprogramming, culture, and differentiation techniques
  • High-throughput and high-content methodologies in hiPSC-based screening

For lab information and more, see Dr. Burridge’s faculty profile and lab website.


See Dr. Burridge's publications on PubMed.


Contact Dr. Burridge at 312-503-4895.

Lab Staff

Postdoctoral Fellows

Brian Burmeister, Zhengxin Jiang, Tarek Mohamed, Adam Schuldt

Graduate Students

Stewart Pine, Mohammed Shereef, Marisol Tejeda

Technical Staff

Defne Egecioglu, Hui-Hsuan Kuo

 Al George Lab

Investigating the structure, function, pharmacology and molecular genetics of ion channels and channelopathies

George Lab

Research Description

Ion channels are ubiquitous membrane proteins that serve a variety of important physiological functions, provide targets for many types of pharmacological agents, and are encoded by genes that can be the basis for inherited diseases affecting the heart, skeletal muscle and nervous system.

Dr. George's research program is focused on the structure, function, pharmacology, and molecular genetics of ion channels. He is an internationally recognized leader in the field of channelopathies based on his important discoveries on inherited muscle disorders (periodic paralysis, myotonia), inherited cardiac arrhythmias (congenital long-QT syndrome) and genetic epilepsies. Dr. George’s laboratory was first to determine the functional consequences of a human cardiac sodium channel mutation associated with an inherited cardiac arrhythmia. His group has elucidated the functional and molecular consequences of several brain sodium channel mutations that cause various familial epilepsies and an inherited form of migraine. These finding have motivated pharmacological studies designed to find compounds that suppress aberrant functional behaviors caused by mutations.

Recent Findings

  • Discovery of novel, de novo mutations in human calmodulin genes responsible for early onset, life threatening cardiac arrhythmias in infants, and elucidation of the biochemical and physiological consequences of the mutations.
  • Demonstration that a novel sodium channel blocker capable of preferential inhibition of persistent sodium current has potent antiepileptic effects.
  • Elucidation of the biophysical mechanism responsible for G-protein activation of a human voltage-gated sodium channel (NaV1.9) involved in pain perception.

Current Projects

  • Investigating the functional and physiological consequences of human voltage-gated sodium channel mutations responsible for either congenital cardiac arrhythmias or epilepsy.
  • Evaluating the efficacy and pharmacology of novel sodium channel blockers in mouse models of human genetic epilepsies.
  • Implementing high throughput technologies for studying genetic variability in drug metabolism.
  • Implementing automated electrophysiology as a screening platform for ion channels.

For lab information and more, see Dr. George’s faculty profile.


See Dr. George's publications on PubMed.


Contact Dr. George at 312-503-4892.

Lab Staff

Research Faculty

Lynn DoglioVladimir Jovasevic, Andrew Mazar, Franck PotetMegan Roy-PuckelwartzChristopher Thompson,Carlos Vanoye

Senior Researchers

Reshma Desai, Jean-Marc DekeyserPaula FriedmanChristine Simmons

Lab Manager

Tatiana Abramova

Postdoctoral Fellows

Thomas HolmDina Simkin

Medical Resident

Tracy Gertler

Graduate Students

Lisa Wren

Technical Staff

Katarina Fabre

 Asish Ghosh Lab

Investigating the epigenetic regulation of cardiac fibrogenesis by acetyltransferase p300, with an emphasis on developing translational therapies.

Research Description

Fibrosis is a common, yet complex, pathophysiological symptom of a wide spectrum of diseases including hypertension and diabetes-associated cardiovascular complications that leads to heart failure. Fibrosis is a major cause of disease-related morbidity and mortality worldwide. Fibrogenic responses are characterized by an excessive accumulation of disorganized extracellular matrix proteins in stressed or injured tissues that leads to loss of tissue elasticity and ultimately, organ failure. There is currently no effective therapy available for fibrotic disorders.

Research in Dr. Ghosh’s lab focuses on understanding the role of factor acetyltransferase p300 (FATp300), a major epigenetic regulator, in extracellular matrix protein collagen synthesis and organ fibrosis. Dr. Ghosh’s research program has demonstrated and described the following novel findings which illustrate fibrogenesis as an epigenetic event:

  • Epigenetic regulator FATp300 is essential for profibrogenic signal-induced elevated collagen synthesis by activated and differentiated myofibroblasts: genetic ablation or pharmacological inhibition of acetyltransferase activity of FATp300 blunts profibrogenic signal-induced collagen synthesis, the major matrix protein contributing to reactive (stress-induced) and reparative (injury-induced) fibrosis.
  • Dissociation of FATp300 from profibrogenic signal-induced transcriptional complex formed on collagen gene promoter through activation of Stat1aor PPAR-gor p53 or small peptide SIDII is an alternative approach to block excessive collagen synthesis in a profibrogenic milieu.
  • The levels of FATp300 and acetylated histones are significantly elevated in myofibroblasts derived from resident fibroblasts or vascular endothelial cells and different fibrotic tissues derived from murine models of fibrosis and heart failure patients. 

Current Projects

  • Investigating the molecular basis of FATp300 elevation in fibrotic cardiac tissues
  • Examining the role of FATp300 in myofibroblast differentiation of resident cardiac fibroblasts and vascular endothelial cells
  • Investigating the contribution of elevated level of FATp300 in cardiac fibrogenesis 
  • Evaluating the therapeutic efficacies of small molecule inhibitors of FATp300 in prevention and reversal of cardiac fibrosis and abnormal cardiac structure/functions in hypertension-induced murine models of cardiac fibrosis.

For more information, see Dr. Ghosh's faculty profile.


See Dr. Ghosh's publications in PubMed.


Contact Dr. Ghosh at 312-503-2150

 Francis Klocke

His research focuses on coronary circulation and cardiac magnetic resonance imaging.

His research focuses on coronary circulation and cardiac magnetic resonance imaging.

Faculty Profile

Francis J Klocke, MD

 Tsutomu Kume Lab

The Kume Lab’s research interests focus on cardiovascular development, cardiovascular stem/progenitor cells, and angiogenesis.

Research Description

Cardiovascular development is at the center of all the work that goes on in the Kume lab. The cardiovascular system is the first functional unit to form during embryonic development and is essential for the growth and nurturing of other developing organs. Failure to form the cardiovascular system often leads to embryonic lethality, and inherited disorders of the cardiovascular system are quite common in humans. The causes and underlying developmental mechanisms of these disorders, however, are poorly understood. A particular emphasis in our laboratory has recently been the study of cardiovascular signaling pathways and transcriptional regulation in physiological and pathological settings using mice as animal models, as well as embryonic stem (ES) cells as an in vitro differentiation system. The ultimate goal of our research is to provide new insights into the mechanisms that lead to the development of therapeutic strategies designed to treat clinically relevant conditions of pathological neovascularization.


View Dr. Kume's publications on PubMed.

For more information, visit the faculty profile for Tsutomu Kume, PhD.

Contact Us

Contact Dr. Kume at 312-503-0623 or the Kume Lab at 312-503-3008.

Staff Listing

Austin Culver
MD Candidate

Anees Fatima
Research Assistant Professor

Christine Elizabeth Kamide
Senior Research Technologist

Erin Lambers
PhD Candidate

Ting Liu
Senior Research Technologist

Jonathon Misch
Research Technologist

 Daniel Lee Lab

Focusing on both the technical development and clinical application of cardiovascular magnetic resonance imaging (CMR).

Dr. Lee's research laboratory focuses on both the technical development and clinical application of cardiovascular magnetic resonance imaging (CMR). His research centers on the following areas:

Viability imaging

 Initial research efforts focused on validating this technique’s ability to measure the extent of myocardial infarction and myocardial viability. Current investigations explore its use as a tool to measure, salvage, and predict remodeling following myocardial infarction, identify patients at risk for ventricular arrhythmias, and gauge the effect of experimental therapies on infarct size.

Myocardial Perfusion Imaging

Our research has demonstrated that first-pass magnetic resonance perfusion imaging has advantages over traditional radionuclide imaging for detecting modest reductions in myocardial blood flow and subtle differences between endocardial and epicardial flow. Investigators in our laboratory are currently developing techniques to measure absolute myocardial blood flow (in mL/min/g), which may allow more precise determination of blood flow limitations. These new techniques are and will be employed to characterize myocardial blood flow in patients with coronary artery disease, microvascular dysfunction, heart failure, and in studies of drug and stem cell therapy.

CMR Core Laboratory

CMR noninvasively obtains high-resolution images with excellent depiction of blood, infarct, and myocardial borders resulting in high reproducibility of measurements.  Not surprisingly, CMR is increasingly being used in clinical trials to quantify left ventricular volumes, mass, and infarct size.

For more information, please see Dr. Lee's faculty profile


See Dr. Lee's publications in PubMed.


Dr. Lee

 Edward Thorp Lab

The Thorp laboratory studies how immune cells coordinate tissue repair and regeneration under low oxygen, such as after a heart attack.

Research Interests

The Edward Thorp Lab studies the crosstalk between immune cells and the cardiovascular system, and in particular, within tissues characterized by low oxygen tension or associated with dyslipidemia, such as during myocardial infarction. In vivo, the lab interrogates the function of innate immune cell phagocytes, including macrophages, as they interact with other resident parenchymal cells during tissue repair and regeneration. Within the phagocyte, the influence of hypoxia and inflammation on intercellular and intracellular signaling networks and phagocyte function are studied in molecular detail. Taken together, our approach seeks to discover and link basic molecular and physiological networks that causally regulate disease progression, and in turn are amenable to strategies for the amelioration of cardiovascular disease.


For additional information, visit the Thorp Lab site or view the faculty profile of Edward B Thorp, PhD.

View Dr. Thorp's publications at PubMed


Contact the Thorp lab at 312-503-3140.

Lab Staff

Shirley Dehn
PhD student

Xin-Yi Yeap, MS
Lab Manager and Microsurgery

 Douglas E. Vaughan Lab

Plasminogen activator system in cardiovascular disease

Research Description

Dr. Vaughan directs a multidisciplinary research group focused on investigating the role of the plasminogen activator system in cardiovascular disease. Active experimental programs are underway at the molecular and cellular level in animals and in humans. Transgenic and knockout mice are used in a variety of studies designed to explore the tissue-specific expression of PAI-1 in vivo and the role of the fibrinolytic system in vascular disease and tissue remodeling.

For more information visit Dr. Vaughan's faculty profile page.


View Dr. Vaughan's publications at PubMed.


Email Dr. Vaughan

Lab Staff

Graduate Students

Varun Nagpal
Rahul Rai

 J. Andrew Wasserstrom Lab

The Wasserstrom Lab studies how intracellular calcium cycling occurs in normal heart cells and how it changes during development of heart disease.

New evidence suggests that heart failure (HF) develops as the result of t-tubule remodeling in response to intracellular signaling during hypertension. The result is a change in intracellular Ca2+ cycling that underlies both diastolic and systolic dysfunction which eventually leads to HF. The lab investigates the molecular basis for t-tubule remodeling and how this leads to impaired Ca2+ cycling during the development of HF. The techniques currently in use in the lab include physiological measurements of intracellular Ca2+ cycling in isolated myocytes and in intact whole hearts using confocal microscopy, molecular techniques including RT- and QT-PCR, viral constructs and knock-out mice, biochemical techniques (Western blot) and immunohistochemistry in order to study the molecular and structural changes responsible for t-tubule loss and subsequent HF development.

A second project is investigating how a specific form of abnormal Ca2+ cycling found primarily in atrial myocytes, called triggered Ca2+ waves, might be responsible for the initiation of atrial fibrillation (AF). This novel form of intracellular Ca2+ cycling is characterized by propagated Ca2+ release events (waves) that occur only during rapid pacing and are absent immediately after pacing, distinguishing them from traditional spontaneous Ca2+ waves that occur exclusively during diastole. Interestingly, findings have indicated that triggered waves develop in tissues with little or no t-tubules including normal atrial myocytes and ventricular myocytes from failing hearts, suggesting an underlying structural basis for this form of potentially arrhythmogenic behavior. Most importantly, these triggered events are also more prevalent in atrial myocytes from failing hearts which could provide an explanation for why failing hearts are more susceptible to the development of AF than non-failing hearts.


View lab publications via PubMed.

For lab information, publications, and more, see Dr. Wasserstrom’s faculty profile.

Contact Us

Contact Dr. Wasserstrom at 312-503-1384 or the Wasserstrom Lab at 312-503-3989.

Lab Staff

Gary Aistrup, PhD
Research Associate Professor

Georg Gussak, MS
Post-graduate Research Fellow

William Marszalec, PhD
Research Assistant Professor

Chloe Monnier, MS
Post-graduate Research Fellow

 Lisa Wilsbacher Lab

The Wilsbacher Lab investigates the roles of G protein-coupled receptors in heart development and disease.

Dr. Wilsbacher's research focuses on cardiac development and cardiomyocyte maintenance in the setting of pathological stress. Currently, the laboratory investigates the G protein-coupled receptor sphingosine-1-phosphate receptor 1 (S1P1) and its unexpected role in cardiomyocyte proliferation and cardiac development. Dr. Wilsbacher’s research aims to identify the signaling mechanisms that underlie these cardiac developmental effects and their potential roles in congenital heart disease. In addition, the laboratory explores whether and how S1P1 signaling contributes to cardiac remodeling in the adult heart, particularly in the setting of cardiac fibrosis.


View lab publications via PubMed.

For more information, visit Dr. Wilsbacher's faculty profile or visit the Lisa Wilsbacher Lab Site.

Contact Us

Contact Dr. Wilsbacher at 312-503-6880 or the Wilsbacher Lab at 312-503-5309.

Lab Staff

Jayne Wolfe
Research Technologist II

Bisheng Zhou
Postdoctoral Fellow

 Ming Zhao Lab

The Zhao lab develops diagnostic markers and investigates pathogenic mechanisms of human diseases based on changes in cellular membranes.

Research Description

Major research areas in the Zhao lab include:

  1. Apoptosis imaging technology development. Programmed cell death (apoptosis) plays a significant role in degenerative diseases. There is currently no clinical tool for assessing apoptosis in pathological conditions. Our research focuses on the development of optimal agents that combine sophisticated binding activities and favorable clearance kinetics for clinical translation.
  2. Assessing systemic toxicity in anticancer therapies. The outcome of chemotherapies hinges on the balance between tumor toxicity and patient tolerance. With the ability to noninvasively detect tissue apoptosis, we propose to assess anticancer therapies in a whole-body approach by monitoring tumor cell killing simultaneously with systemic tissue injury in response to chemotherapeutic agents. This is a transformative approach in oncology in terms of optimizing therapies on an individualized basis.
  3. Detecting myocardial injury in ischemic heart disease. Non-infarct myocardial injury in ischemic heart disease is of particular interest because this type of cardiac injury is not well understood in terms of its pathophysiological characteristics and its roles in long-term adverse cardiac events. Our research in this area focuses on the diagnosis of non-infarct myocardial injury, which in turn, will help address a significant gap in identifying patients at risk.
  4. Investigating the pathogenesis of antiphospholipid syndromes. The presence of circulating antibodies against phosphatidylethanolamine (PE) is positively correlated with clinical manifestations of antiphospholipid syndromes. However, the underlying pathogenic mechanism of anti-PE autoimmunity remains unknown. We have a major interest in investigating the cellular susceptibility to PE-binding agents, which in turn, will shed light on the potential pathogenic mechanism of aPE.


View publications by Ming Zhao in PubMed.

For more information, visit Dr. Zhao's Faculty Profile page


Contact Dr. Zhao at 312-503-3226.

Lab Staff

Songwang Hou, PhD
Research Associate

Steven E. Johnson
Graduate Student

Ke Ke, PhD
Research Associate

Kaixi Ren, MD
Graduate Student