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Cardiovascular System

Research into the development, physiologic functions and disease of the cardiovascular systems. Many of the investigators listed here also belong to the Feinberg Cardiovascular Research Institute.

Labs in This Area

 Hossein Ardehali Lab

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


Research Description

Our lab focuses on three major areas of research:

Role of hexokinase enzymes in immune function, cancer growth and stem cell differentiation

Hexokinase (HK) enzymes phosphorylate glucose to trap it inside the cell. There are 5 mammalian HKs (named HK1-5), with two of them having a hydrophobic region at their N-terminus that allows them to bind to the mitochondria. We have made mouse models and developed in vitro systems to allow us to study the role of mitochondrial binding of HKs in glucose metabolism. We have determined that HK1 binding to the mitochondria determines whether glucose is used for anabolic processes (ie, pentose-phosphate pathway) or catabolism (ie, glycolysis). Thus, the non-enzymatic function of this protein and its subcellular location determines the fate of glucose. We are now studying this process in T-cells, vascular cells and cancer cells. We are also in the process of generating several mouse models of hexokinase enzymes, including HK2 without the mitochondrial binding domain and HK3 knockout mice. We will study these models in different disease and physiological conditions.

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 through epigenetic changes, 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.

Role of mRNA-binding proteins 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. 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.

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.


The primary focus of the Arora lab is to obtain a better understanding of the molecular mechanisms underlying heart rhythm disorders (cardiac arrhythmias). The cardiac arrhythmia most closely studied in the Arora lab is atrial fibrillation (AF). AF is the most common rhythm disorder of the heart that affects >6 million American and is a major cause of stroke. Unfortunately, current therapies for AF have suboptimal efficacy. This is thought to be because current therapies are not targeted at the major molecular mechanisms underlying AF. The focus of research in the Arora lab has therefore been to not only better understand the molecular mechanisms underlying AF but to discover new, mechanism-guided therapies for this condition. Dr. Arora’s laboratory is one of the few in the world dedicated to understanding the molecular mechanisms underlying AF and to translating these research findings to the clinic.

Over the last 15 years, the Arora lab has discovered that autonomic nervous system signaling, oxidative injury, altered excitation-contraction coupling and TGF-β signaling are key mechanisms underlying the genesis of AF. Because AF is predominantly a disorder of the larger, mammalian heart, the Arora lab laboratory primarily uses large animal models of AF to understand mechanisms of AF. Over the last few years, the Arora lab has developed new gene-based therapies for this condition. This has included not only the gene-based targeting of key molecular signaling pathways underlying AF, but has also included the development of new devices and energy sources (such as electroporation) to perform targeted gene delivery in the heart.

In its quest to develop new, mechanism guided therapies for AF, the Arora lab is also engaged in the development of new, signal processing algorithms to study the electrical signals (electrograms) in the fibrillating heart. Over the last several years, the lab have published many papers on how AF electrograms can be used to determine pathophysiological substrate for AF.

Dr. Arora has mentored more than 40 trainees in his lab over the last 17 years, and currently serve as training director on a major grant from the American Heart Association. The lab is an ideal home for graduate students interesting in the following areas of biology:

Cardiovascular physiology, with a focus on cardiac electrophysiology: The lab uses a variety of cutting edge techniques to study the electrophysiology of the heart from cell-to-bedside. This includes high resolution electrophysiological mapping in the intact heart (in-vivo), high resolution optical mapping in the explanted heart (ex-vivo) and cellular electrophysiological techniques in isolated cardiomyocytes to assess excitation contraction coupling (calcium cycling) and whole cell ion channel electrophysiology. Biomedical engineering, instrumentation: The lab uses a variety of signal processing techniques to assess intracardiac electrograms from animals and humans with AF. The lab also investigates the behavior of autonomic nerves in the heart, using digital signal processing. In addition to signal processing, the lab is also actively engaged in the development of new devices (hardware) to perform gene delivery in the heart.

Gene therapy: A major focus of the lab is to develop new gene therapy approaches for cardiac arrhythmias. This includes the identification of novel gene targets in AF, use of new delivery vectors (non-viral and viral) for targeted gene therapy in the heart, and the development of new, catheter-based gene delivery techniques.

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


See Dr. Arora's publications in PubMed.

 Grant Barish Lab

Transcriptional regulators of inflammation and metabolism

Research Description

The burgeoning epidemic of obesity and type 2 diabetes mellitus presents a major health and therapeutic challenge.  Transcriptional regulation is the fundamental control mechanism for metabolism, but a gap remains in our knowledge of gene regulatory pathways that control lipid and glucose homeostasis.  Thus, we seek to identify modulable pathways that may be leveraged to counteract diabetes mellitus and its comorbidities, particularly cardiovascular disease.  In this effort, we use a variety of genetic, molecular, next-generation sequencing, biochemical methods and physiological models.  Our recent work has helped to reveal the genomic architecture for transcriptional regulation in innate immunity, which plays a key role in both diabetes mellitus and atherosclerosis.  Surprisingly, although macrophage regulatory elements are often at significant linear distance from their associated genes, we identified interplay between transcriptional activators and repressors that is highly proximate, occurring at shared nucleosomal domains (Genes & Development, 2010).  Moreover, we discovered a powerful role for the BCL6 transcriptional repressor to maintain macrophage quiescence and prevent atherosclerosis (Cell Metabolism, 2012). 

Currently, we are exploring the impact of activator–repressor interactions on enhancer function and transcription, the signal-dependent control of repression and the functional impact of transcriptional activators and repressors on inflammatory and metabolic disease. In particular, we strive to further understand the role for B cell lymphoma 6 (BCL6), a C2H2-type zinc finger repressor, in innate immunity and metabolism. 

In related work, we are developing new methods for cell-specific isolation of RNA and chromatin from tissues composed of mixed cell populations. These genetic tools will allow us to explore transcriptional regulation in living animals with unprecedented precision and global scope using transcriptome sequencing and ChIP-sequencing. We anticipate that these approaches will identify new candidate regulators and mechanisms underlying cardiovascular and metabolic disease. 

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


See Dr. Barish's publications in PubMed.

Graduate Students

Madhavi Senagolage
Meredith Chase
Krithika Ramachandran


Dr. Barish

 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

Malorie Blancard, Hananeh Fonoudi, Mariam Jouni, Davi Leite, Tarek Mohamed, Disheet Shah

Graduate Students

Liora Altman-Sagan, Raymond Copley, K. Ashley Fetterman, Phillip Freeman, Donald McKenna, Emily Pinheiro, Marisol Tejeda, Carly Weddle

Technical Staff

Ali Negahi Shirazi

 Matthew Feinstein Lab

Adaptive Immune Response and Regulation in Cardiovascular Diseases 

Research Description

Our lab focuses on clinical and translational immunocardiology. The central approach we use is one of reverse translation: This enables us to take insights from human phenotypes and models of disease, test and refine these insights and hypotheses in experimental models, and ultimately bring these insights to clinic. Leveraging our expertise in clinical and epidemiological research as well as translational and basic investigation, we utilize techniques including single-cell RNA-seq, spatial sequencing (in myocardial and vascular tissue), cutting edge tissue visualization techniques, and traditional immune phenotyping methods (e.g. flow cytometry) to probe the immunopathogenesis of specific cardiovascular diseases (CVDs). To support our investigation of these tissue- and disease-specific processes, we have linked complex individual-level clinical data to stored FFPE tissue specimens from >2000 patients who underwent autopsy, enabling interrogation of multi-organ interactions in the immunopathogenesis of CVDs. We developed the first model of closed-chest ischemia-reperfusion injury in nonhuman primates and use this to interrogate local and peripheral immune responses to myocardial ischemia and infarction in immune-competent and immune-dysregulated models. After we generate target- and tissue-specific hypotheses in human and large animal models, our close collaboration with the Thorp Lab through our shared Clinical and Translational Immunocardiology Program ( enables us to experimentally probe processes of interest in small animal and in-vitro models, then ultimately bring these insights and potential therapies to NHP models and back to humans.   

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


View Dr. Feinstein's full list of publications on PubMed.

Contact Us

Matthew Feinstein, MD 


 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

Irawati Kandela, Thomas Lukas, Christopher Thompson, Carlos Vanoye

Senior Researchers

Reshma Desai, Jean-Marc DekeyserPaula FriedmanChristine Simmons

Lab Manager

Tatiana Abramova

Postdoctoral Fellows

Dina Simkin

Medical Residents

Scott Adney, Tracy Gertler

Graduate Students

Huey Dalton, Surobhi Ganguly, Adil WafaLisa Wren

Technical Staff

Nora Ghabra, Nirvani Jairam

 Luisa Iruela-Arispe Lab

Molecular regulation of angiogenesis and vascular homeostasis

Research Description

Currently, the laboratory is investigating the mechanisms behind the formation of vascular tumors and vascular anomalies. In particular, the group is interested in the identification of critical regulatory nodes that maintain vascular homeostasis and control endothelial proliferation in the context of flow. An additional focus of the lab is to dissect the molecular interactions between endothelial and tumor cells during the process of metastasis with particular emphasis on endothelial barrier.

For lab information and more, see Dr. Iruela-Arispe's faculty profile.


See Dr. Iruela-Arispe's publications on PubMed.


Email Dr. Iruela-Arispe



 Bin Jiang Lab

Vascular disease modeling, tissue engineering and regenerative medicine

Research Interests

The Jiang laboratory is an interdisciplinary research program of vascular surgery and biomedical engineering. The primary focus of our work is on vascular repair and regeneration for a variety of vascular diseases and conditions. We use a combination of innovative technologies, including induced pluripotent stem cells (iPSCs), biomaterials, and non-invasive imaging to develop patient-specific, tissue engineered vascular constructs. Currently, the laboratory is investigating the mechanisms behind vascular calcification and abdominal aortic aneurysm with novel disease models in vitro and in vivo. Additionally, we explore the role of microenvironment in the differentiation of vascular cell phenotypes in health and disease. Ultimately, the scientific discoveries and engineering solutions developed by our research program will benefit patients suffering from vascular diseases.

For more information, visit Dr. Jiang's faculty profile page or the Jiang lab website


See Dr. Jiang's publications.


Dr. Jiang

 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

 Jennie Lin Lab

The Lin lab studies the functional significance of human-based genomic and transcriptomic discoveries in cardiometabolic and kidney diseases.

Research Description

Elucidating How Genotype Lease to Phenotype in Cardiometabolic and Renal Disease

Unbiased human-based discovery efforts, such as genome-wide and exome-wide association studies, have identified many genetic loci for complex, disease-relevant traits. These genetics studies have provided invaluable data implicating novel loci in disease development and progression, but require functional follow-up to elucidate the mechanistic underpinnings driving the associated findings. A focus of the lab is to interrogate, through experimental wet-bench approaches, the functional significance of novel loci for blood lipids levels and measurements of renal function in the hopes of gaining new insights into pathways relevant to cardiometabolic and renal disease, respectively.

In particular, we are studying the role of A1CF, a gene encoding the RNA-binding protein APOBEC1 complementation factor and recently implicated as a locus for (1) elevated plasma triglycerides (Liu et al., Nature Genetics 2017), (2) estimated glomerular filtration fraction in non-diabetic individuals (Pattaro et al., Nature Communications 2016) and (3) serum urate (Kottgen et al., Nature Genetics 2013). We have already discovered that A1CF's actions extend beyond its canonical role of facilitating the editing of APOB mRNA, and we are currently integrating studies using animal and human cellular models to investigate how A1CF contributes to these associated traits.

Using iPSC and Genome Editing Technologies to Study Human Diseases

Although rodent models have contributed greatly to our understanding of human diseases, the genomic and physiologic differences between rodent and human have presented challenges in translating bench-based findings into clinic. To circumvent this roadblock, our lab is using iPSC-derived organoid models to study the effects of DNA variants within the native human genomic context. Using CRISPR-based technology to introduce or correct mutations in human iPSCs, we are modeling the effects of disease-associated mutations on cellular phenotype.

RNA-centric Approach to Studying Kidney Disease

Building upon A1CF-related work and previous experience with long non-coding RNA, we are studying the role of transcriptome-level regulation in the context of kidney disease. We have discovered that A1CF is a novel regulator of alternative splicing in both the liver and kidney, and we are currently working on how A1CF's regulation of splicing may influence intracellular metabolism. We are also studying how human-specific long non-coding RNAs influence gene expression and cellular phenotypes.

For more information, visit the Faculty Profile of Jennie Lin or visit the Lin Lab Website


See Dr. Lin's publications in PubMed.


Email Dr. Lin

Phone 312-503-1892

 Donald Lloyd-Jones Lab

Cardiovascular disease epidemiology, risk estimation and prevention

Research Description

Dr. Lloyd-Jones’ research interests lie in cardiovascular disease epidemiology, risk estimation and prevention. A main focus of his research has been investigation of the lifetime risks for various cardiovascular diseases and factors that modify those risks. Other areas of interest include cardiovascular disease risk estimation using novel biomarkers, imaging of subclinical atherosclerosis and the epidemiology of hypertension. His clinical and teaching interests lie in general cardiology with a focus on prevention.

For more information, visit the faculty profile of Donald Lloyd-Jones, MD, ScM.


Email Dr. Lloyd-Jones

Phone 312-908-1718

 Aline Martin Lab

The Martin Lab investigates the role of the skeleton in the endocrine regulation of mineral metabolism and the cardiovascular complications of mineral and bone diseases.

Our research program focuses on the contribution of the skeleton to the mineral balance in the body.  Bone produces a hormone, Fibroblast Growth Factor (FGF)-23, that participates in this balance.  However in mineral metabolism disorders, such as in chronic kidney disease, the massive production of FGF23 is associated with negative outcomes and mortality.  By understanding the mechanisms that control the production of FGF23, our goal is to develop new therapeutic strategies and improve outcomes in mineral metabolism disorders.  To this goal, we perform basic and translational research using a combination of genetics, molecular biology, proteomics, histology and advanced imaging techniques. 

A major focus of the lab is to investigate the transcriptional and post-translational regulation of FGF23 within the bone cells.  In particular, we study the specific role of a known regulator of FGF23, Dentin Matrix Protein 1 (DMP1), on these regulations and on osteocyte biology in the context of diseases associated with FGF23 excess (chronic kidney disease, hypophosphatemic rickets …).  A second focus is to investigate the mechanisms involved in negative outcomes associated with FGF23 excess, including bone mineralization defects, cardiac hypertrophy and cognitive defects.  Our team works in collaboration with the Center for Translational Metabolism and Health and the Division of Cardiology at Northwestern, and with multiple additional collaborators and partnerships around the world.

The Martin Lab is sponsored by the National Institute of Health, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and by the Northwestern Women’s Health Research Institute.


For more information view Dr. Martin's Faculty Profile or  view publications by PubMed

Contact Us

Contact Dr. Martin at 312-503-4160 or the Martin Lab at 312-503-4805, or by email.

 Elizabeth McNally Lab

Genetic mechanisms responsible for inherited human diseases

Research Description

My laboratory studies genetic mechanisms responsible for inherited human diseases including heart failure, cardiomyopathy, muscular dystrophy, arrhythmias, aortic aneurysms. Working with individuals and families, we are defining the genetic mutations that cause these disorders. By establishing models for these disorders, we can now begin to develop and test new therapies, including genetic correction and gene editing.

For lab information and more, see Dr. McNally's faculty profile or visit the McNally Laboratory site.


See Dr. McNally's publications on PubMed.


Email Dr. McNally

Phone  312-503-5600

 Susan Quaggin Lab

Uncovering the molecular mechanisms of diabetic vascular complications, thrombotic microangiopathy, glomerular diseases and glaucoma

Our lab focuses on the basic biology of vascular tyrosine kinase signaling in development and diseases of the blood and lymphatic vasculature.  Our projects include uncovering the molecular mechanisms of diabetic vascular complications, thrombotic microangiopathy, glomerular diseases and glaucoma.  Utilizing a combination of mouse genetic, cell biologic and proteomic approaches, we have identified key roles for Angiopoietin-Tie2 and VEGF signaling in these diseases.  Members of the lab are developing novel therapeutic agents that target these pathways.  

For more information, please see the faculty profile of Susan Quaggin, MD


See Dr. Quaggin's publication in PubMed


Email Dr. Quaggin

 Benjamin Thomson Lab

Links between endothelial function and vision

Research Interests

Endothelial dysfunction is a major cause of vision loss, playing a key role in diseases including age-related macular degeneration, diabetic retinopathy and glaucoma. Using mouse genetics, animal disease models and a combination of single cell RNA-sequencing and histological approaches, our lab is focused on understanding the role of the vasculature in these diseases, including glaucoma and age related macular degeneration. By elucidating molecular connections between endothelial dysfunction and vision loss, we aim to identify novel therapeutic targets and translate these discoveries into patient care.

While endothelial dysfunction is a component of many eye diseases, the importance of ocular vasculature in age related macular degeneration is widely understood and is the basis for the life-altering anti-VEGF therapies that target choroidal neovascularization associated with these conditions. The choroid and choriocapillaris (CC) form a unique vascular bed in the back of the eye that is vital for maintenance of the retinal photoreceptors and retinal pigment epithelium (RPE). In addition to the well-described link with AMD, choroidal dysfunction is tied to the poorly understood spectrum of pachychoroid diseases including polypoidal choroidal vasculopathy (PCV), which can lead to irreversible loss of vision. Despite their clinical impact, little is known about pathogenesis or optimal treatment of PCV and other pachychoroid diseases, or why some patients with defects in the choroidal vasculature develop geographic atrophy or neovascular AMD and others PCV. Ongoing research in our lab seeks to answer this question, using animal models, single cell RNA sequencing and in vivo imaging to gain mechanistic insights into pachychoroid biology, understand mechanisms by which choriocapillaris attenuation lead to choroidal dysfunction, and identify genes and pathways which can be targeted for future therapies. 


For additional information, visit the faculty profile of Dr. Thomson

View Dr. Thomson's publications at PubMed


Contact Dr. Thomson


 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

Shuang Zhang
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

 Youyang Zhao Lab

The Zhao Lab studies the molecular mechanisms of endothelial regeneration and resolution of inflammatory injury as well as endothelial and smooth muscle cell interaction in the pathogenesis of pulmonary vascular diseases.

Research Description

Recovery of endothelial barrier integrity after vascular injury is vital for endothelial homeostasis and resolution of inflammation. Endothelial dysfunction plays a critical role in the initiation and progression of vascular diseases such as acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and atherosclerosis. A part of the research in the lab, employing genetically modified mouse models of human diseases, endothelial progenitor cells/stem cells, and translational research approach as well as nanomedicine, is to elucidate the molecular mechanisms of endothelial regeneration and resolution of inflammatory injury and determine how aging and epigenetics regulate these processes (J. Clin. Invest. 2006, 116: 2333; J. Exp. Med. 2010, 207:1675; Circulation 2016, 133: 2447).  We are also studying the role of endothelial cells in regulating macrophage functional polarization and resolving inflammatory lung injury. These studies will identify druggable targets leading to novel therapeutic strategies to activate the intrinsic endothelial regeneration program to restore endothelial barrier integrity and reverse edema formation for the prevention and treatment of ARDS in patients.

Pulmonary hypertension is a progressive disease with poor prognosis and high mortality. We are currently investigating the molecular basis underlying the pathogenesis.  We have recently identified the first mouse model of pulmonary arterial hypertension (PAH) with obliterative vascular remodeling including vascular occlusion and formation of plexiform-like lesions resembling the pathology of clinical PAH (Circulation 2016, 133: 2447). Our previous studies also show the critical role of oxidative/nitrative stress in the pathogenesis of PAH as seen in patients (PNAS 2002, 99:11375; J. Clin. Invest. 2009, 119: 2009). With these unique models and lung tissue and cells from idiopathic PAH patients, we will define the molecular and cellular mechanisms underlying severe vascular remodeling and provide novel therapeutic approaches for this devastating disease. 

The Zhao lab employs the state-of-the art technologies including genetic lineage tracing, genetic depletion, genetic reporter, and CRISPR-mediated in vivo genomic editing as well as patient samples to study the molecular mechanisms of acute lung injury/ARDS, and pulmonary hypertension and identify novel therapeutics for these devastating diseases. Current studies include 1) molecular mechanisms of endothelial regeneration and vascular repair following inflammatory lung injury induced by sepsis and pneumonia; 2) how aging and epigenetics regulate this process; 3) how endothelial cells regulate macrophage and neuptrophil function for resolution of inflammation and host defense; 4) stem/progenitor cells in acute lung injury and pulmonary hypertension and cell-based therapy; 5) mechanisms of obliterative pulmonary vascular remodeling; 6) molecular basis of right heart failure; 7) pathogenic role of oxidative/nitrative stress; 8) lung regeneration; 9) drug discovery; 10) nanomedicine.


View publications by Youyang Zhao in PubMed.

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


Email Dr. Zhao

Contact Dr. Zhao’s Lab at 773-755-6355

Lab Staff

Zhiyu Dai, PhD.
Research Assistant Professor

Xianming Zhang, PhD.
Research Assistant Professor

Narsa Machireddy, PhD.
Research Assistant Professor

Junjie Xing, PhD.
Research Scientist

Colin Evans, PhD.
Research Scientist

Varsha Suresh Kumar, PhD.
Research Scientist

Xiaojia Huang, PhD
Research Scientist

Hua Jin, PhD
Postdoctoral fellow

Yi Peng, PhD
Research Scientist

Mengqi Zhu, M.S.,
Graduate Student

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