AHA SURE MENTORS

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(click on the mentor's name to view their profile and link to their lab)

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Karen Stokes, PhD - (Principle Investigator and mentor) 
The Stokes lab focuses on the intersection between inflammation and thrombosis in stroke (under diabetic conditions and in sickle cell disease), and on the role for redox regulation in vascular changes in Alzheimer's Disease.

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Matthew Woolard, PhD - (Co-Investigator and mentor)
The Woolard lab is focused on understanding the contribution of immune system to atherosclerotic progression, the number one cause of catastrophic cardiovascular disease. Specifically we are determining how lipid metabolisms within macrophages contributes to both promotion of atherosclerotic plaque growth and plaque regression. Understanding the intersection of immunometabolic responses and atherosclerosis will identify new therapeutic targets to reduce the burden of cardiovascular disease.

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Mabruka Alfaidi, MD, PhD
Coronary Artery Disease (CAD) is a leading cause of disease death worldwide. Despite our technical advances, finding a cure is still challenging. In our research group we explore the intra-molecular pathways in individual cellular responses using translational tools from patients with or without CAD to small and large animal-based approaches.

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Md Shenuarin Bhuiyan, PhD
The Bhuiyan lab focus is to examine the role of autophagy in cardiac pathophysiology using integrated molecular, genetic, and functional approaches in genetically modified mice. My laboratory extensively uses cardiac-specific transgenic and knockout mouse models of heart failure including ischemia/reperfusion injury-, transverse aortic constriction- and genetic models (desmin related cardiomyopathy) of heart failure.

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Nirav Dhanesha, PhD
The Dhanesha lab applies a multidisciplinary approach in stroke and thrombosis research, combining data from human samples, in vitro assay and preclinical models of stroke, venous and arterial thrombosis. Current focus of the lab includes understanding of the mechanistic role of neutrophil integrin alpha9beta1 in the pathogenesis of venous thrombosis in the setting of stroke and obesity.

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Chris Kevil, PhD
The Kevil lab focuses on hydrogen sulfide and its enzymes in the regulation of vascular remodeling, inflammation in diabetes and autophagy.

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Jeremy Kamil, PhD
The Kamil laboratory is broadly interested in how viruses enter cells, regulate their genes, and rewire host cells to serve their interests. A more recent focus of the lab concerns how viruses commandeer host cell machinery to coat their virions in sialic acid containing glycans that restrain antiviral activities of immune cells. To address these questions, we study human cytomegalovirus (HCMV), a complex and fascinating large DNA virus that infects approximately half of the human population. Tragically, HCMV is a leading cause of dangerous infections in immunocompromised people, and is also a major threat to the developing fetus during pregnancy. Overall, the laboratory leverages molecular genetics and cell biology to explore fundamental aspects of virus biology. We are honored to contribute to the development of vaccines and therapies to prevent HCMV related diseases

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Tarek Magdy, PhD 
The Magdy laboratory is trying to understand the role of the genome in patient-specific drug response and cardiovascular disease predisposition. We are particularly interested in the pharmacogenomics of chemotherapy-induced cardiotoxicity and congenital heart diseases using human-induced pluripotent stem cells-derived cardiomyocytes (hiPSC-CMs). To do this, we adopt state-of-the-art techniques, including somatic cell reprogramming into human induced pluripotent stem cells, multi-lineage iPSC differentiation, CRISPR/Cas9-mediated functional genomics methods, multi-omics approaches, and bioinformatics, combined with various quantitative and qualitative in vitro studies.

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A. Wayne Orr, PhD
The Orr lab studies the cellular and molecular mechanisms that drive the formation of atherosclerotic plaques, the most common cause of heart attacks and strokes and the leading cause of death worldwide.  Using vascular cell culture, mouse models, and patient samples, our work identifies novel pathways contributing the buildup of lipids, inflammatory cells, and fibrous tissue in the vessel wall with the ultimate goal of reducing clinical complications of atherosclerosis.

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Changwon Park, PhD
The Park lab long-term goal is to understand the detailed mechanisms of vascular diseases including cardiovascular disease, neurovascular disease, and tumor immunity with a special emphasis on transcriptional regulation and epigenetics. We are also interested in direct cell reprogramming to generate autologous endothelial cells for cell therapy. Further, we are studying novel therapeutic options for vascular disease treatment.

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Chris Pattillo, PhD
The Pattillo lab focuses on the role that reactive oxygen species and antioxidants play on vascular remodeling. Two remodeling events we study are shear induced arteriogenesis and atherosclerosis.

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Krista Rodgers, PhD
Research in the Rodgers lab focuses on the endogenous regeneration of brain cells following stroke, and how these new brain cells contribute to enhanced post-stroke outcomes (i.e., improved motor recovery, reduced limb neglect, improved neuroplasticity/EEG). We have found a role for neuroimmune support in the survival and maturation of new brain cells in young mice compared to adult, and are investigating these age-related differences in immune functioning following stroke.

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Oren Rom, PhD, RD
The long-term goal of Dr. Rom's research program is to elucidate metabolic and molecular mechanisms of cardiometabolic and liver diseases to identify novel therapeutic targets.  The focus of Dr. Rom's laboratory is to shed light on yet undefined metabolic pathways linking cardiovascular disease with metabolic dysfunction-associated steatotic liver disease (MASLD), a disease that affects one third of the world population with no pharmacological therapy available. His lab utilizes a multidisciplinary approach involving newly generated animal models, samples from patients with cardiometabolic diseases and genome‐wide association studies (GWAS) combined with a variety of research tools including transcriptomics, metabolomics, animal pathophysiology as well as cellular and molecular biology. This approach highlighted newly identified metabolic pathways linking amino acid, oxalate, polyamine, and lipid metabolism in MASLD, the more severe metabolic dysfunction-associated steatohepatitis (MASH), and atherosclerosis as potential therapeutic targets, resulting in high-impact publications (Cell Metab, Sci Transl Med, Circulation, Circ Res, Nat Commun, Cell Rep, EBioMedicine, JCI, JCI insight, ATVB, Redox Biol,and Free Radic Biol Med), patent applications (PCT/US19/46025, PCT/US21/46357, PCT/US22/43212, and PCT/US2023/68990), and evaluation through preclinical and clinical trials. 

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Arif Yurdagul, PhD
Despite advances in surgical intervention and cholesterol-lowering drugs over the last few decades, atherosclerotic cardiovascular disease remains the leading cause of death worldwide. Atherosclerosis forms when modified low-density lipoproteins (LDL) accumulate in the subendothelial matrix of medium-sized arteries in areas of branch points, curvatures, and bifurcations, which generate a sustained inflammatory response in endothelial cells and drive leukocyte recruitment. Many of these infiltrating leukocytes become apoptotic, and while these dead cells are efficiently cleared by macrophages (termed “efferocytosis”) early in lesion formation, efferocytosis begins to fail as atherosclerosis progresses, resulting in an overabundance of post-apoptotic dead cells in an area of the atheroma called the necrotic core. In humans, plaques with large necrotic cores and thin fibrous caps are vulnerable to rupture, leading to myocardial infarction and stroke. Therefore, revealing the mechanisms by which efferocytosis fails as atherosclerosis progresses and how efferocytosis is restored during atherosclerosis regression are important objectives in the Yurdagul lab. With these goals in mind, we hope to identify new therapeutic approaches to curb atherosclerotic cardiovascular disease.

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Andrew Yurochko, PhD
Cytomegalovirus can cause vascular disease associated with transplant rejection, and has been implicated in cardiovascular disease. The Yurochko lab is investigating how HCMV infects and utilizes bone marrow progenitor cells and monocytes/macrophages to promote life-long viral persistence and how infection of these cells in vivo contributes to acute and chronic virus-mediated human disease.