Research Advancements

76th Annual Affair of the Heart Luncheon and Fashion Show

Friday, February 9, 2024

Research Advancements

2023 Research Grants

Jocelyn Beard Moran Memorial Fellowship

Hovhannes Arestakesyan, PhD

Postdoctoral Fellow
The George Washington University

Astrocyte senescence and hypertension

The process of “senescence” can cause abnormal cell function in brain cells, also called astrocytes. This process has been observed to occur in the brain cells of mice with high blood pressure. Senescence can also cause neighboring brain cells to not function properly by causing inflammation. These abnormalities and changes in the function of astrocytes can lead to high blood pressure. By examining the details of these changes in mice, we can also test whether correcting senescence in the brain can lower high blood pressure. We hope that our studies will lead to developing drugs that can be used to target senescence and treat high blood pressure.

Anne Davis Camalier Award

Axel Fenwick, PhD

Postdoctoral Fellow
Johns Hopkins University School of Medicine

Determining Ultrastructural Aberrations and Myofibril Kinetics in Human Heart Failure with Preserved Ejection Fraction

To distribute oxygenated blood, the heart cycles through contraction and relaxation, resulting in a heartbeat. When the heart muscle fails to pump blood efficiently, the result is heart failure. In some cases, the heart can contract with normal strength but fails to relax properly. Instead of bouncing back like a spring, it bounces back more like a foam mattress, which limits blood flow. Our research will use advanced ultrasound imaging to understand the machinery that controls the relaxation of the heart muscle on a cellular and subcellular level. This will allow the development of drugs to help relaxation and may later be used in humans to allow their hearts to beat normally.

Donna Graff Marriott Award

Taibo Li, M.Eng.

Predoctoral Fellow
Johns Hopkins University School of Medicine

Dynamic regulatory networks underlying cardiomyocyte differentiation

The heart is the first organ to form in human embryos. Many genes are turned on and off at different stages of heart development in a coordinated manner. Defects in this process can cause congenital heart disease (CHD) leading to pediatric heart disease. Our goal is to study when and how genes work with each other to drive heart development and how some mutations can lead to CHD. By studying how early cells become heart muscle cells, we can analyze data and determine what areas contain key information for heart development. Through this process, we can improve genetic screening of CHD, help drive individualized treatment and shed light on new therapies that repair damaged heart tissue.


Yitao Huang, B.M.

Predoctoral Fellow
University of Virginia

A novel role for aurora kinase B (AURKB) in chromatin remodeling and intimal hyperplasia

Often, after surgical repair of a diseased, blocked section of an artery, there will be a narrowing of the vessel at the repair site, which can lead to a process called “intimal hyperplasia.” This process can disrupt blood flow which can lead to vascular diseases such as heart attack and stroke. Through efforts to repair diseased arteries, we hope our studies will demonstrate other options for the treatment of intimal hyperplasia. One such strategy is to use a protein that plays a role in the cell cycle, called aurora kinase B (AURKB), to repair diseased arteries. We hope our studies will demonstrate other options for the treatment of this disease affecting millions of individuals.

Jose Verdezoto Mosquera

Predoctoral Fellow
University of Virginia

Spatiotemporal regulatory mechanisms of smooth muscle cell phenotypic modulation during atherosclerosis progression

Coronary artery disease (CAD) is caused by a buildup of fat and other substances in blood vessel walls, which can lead to the development of “plaque.” If the plaque becomes unstable and ruptures, it can lead to blood flow blockages which can cause a heart attack or stroke. Our lab studies how smooth muscle cells (SMC) within the blood vessel wall can control the stability of the plaque. We are working to find the DNA-level processes causing SMC behavior shifts and where in the plaque they occur while pinpointing SMCs in plaques using specific gene markers. These findings will help develop new CAD treatments that will help to make plaques more stable, prevent heart attacks and save lives.


2020 Research Grants

2019 AHA Postdoctoral Fellowship
Postdoctoral Fellowship Reseracher
Gamze Bulut, PhD

University of Virginia School of Medicine
Charlottesville, VA

Perivascular smooth muscle derived macrophage-like cells maintain vessel integrity and respond to vascular remodeling

Smooth muscle is an involuntary muscle that lines hollow organs in the body including arteries. The smooth muscle cell (SMC) is the predominant cell type in the middle layer of the aorta and has been shown to undergo observable characteristic changes which can resemble other cells, especially when there is a plaque buildup (or blockage) in the vessel.  SMCs contribute to the protective fibrous cap to prevent rupture of the plaque, which can cause a heart attack.  Our research focuses on how SMCs become macrophage cells, which act like white blood cells that can “patrol” as part of the immune system. We have generated an indicator mouse model wherein SMCs that have become macrophage like will be labeled with green fluorescent protein.  We are interested in learning the function of these green cells with respect to maintaining the integrity of the blood vessels.  Additionally, we have generated another mouse model where we can inject a drug to kill off green cells and observe how vessel integrity, new vessel formation and remodeling will be affected.  Our research will help advance the understanding of the cellular biology of blood vessels.

2019 Established Investigator Award
Established Investigator Researcher

Adam Straub, PhD

University of Pittsburgh
Pittsburgh, PA

Iron Redox Regulation: Basic Mechanisms, Translational Implications and Strategies to Treat Cardiovascular Disease

The chemical role of cellular regulation utilizing iron is known as “iron redox regulation” and is essential to many facets of cardiovascular physiology including maintenance of the integrity of blood vessels as well as production of energy in the heart muscle. Nevertheless, little is known about the specifics of iron regulation in diseases such as hypertension, heart failure and stroke. The goal of the research is to identify unknown iron redox-regulated proteins critical for the integration of genetic, metabolic, and functional processes necessary for cardiovascular function. Additionally, our research will address whether a specific genetic variant in some African-Americans called Cyb5R3 T117S impairs the redox process and increases the risk of heart disease in affected populations. Using a novel screening tool, our research will address these issues and help develop new therapeutic targets, strategies, and drugs to alleviate the physical, mental and financial burdens linked to cardiovascular disease.

2019 AHA Postdoctoral Fellowship
postdoctoral fellowship researcherLaura Payne, PhD

Virginia Polytechnic Institute
Blacksburg, VA

Pericyte cooperation in vessel formation by VEGF-A-regulated production of collagen-III and -IV by endothelial cells

Cardiovascular disease is the leading cause of death worldwide, yet critical questions remain regarding how healthy, stable blood vessels form. In the event of tissue damage or low oxygen, increased levels of Vascular Endothelial Growth Factor-A (VEGF-A) stimulate growth of existing vessels. The extracellular matrix (ECM) surrounding vessels is remodeled to allow endothelial cells (EC), cells which form the vessel wall, and pericytes (PC), cells which stabilize vessels, to form additional vessels. However, if VEGF-A levels remain high, dysfunctional vessels form.  In poorly oxygenated tissues, VEGF-A stimulates new blood vessel growth to re-oxygenate the tissue. However, diseases associated with chronic lack of oxygen, such as ischemic stroke, heart failure, and diabetes, which increase cardiovascular disease risk, cause excess VEGF-A release and defective vessel formation which can lead to tissue loss and disease progression. Recent evidence suggests that pericytes are involved in this process. However, little is known about how VEGF-A influences endothelial and pericyte interactions as well as downstream formation of dysfunctional vessels. Our research seeks to uncover how these cellular interactions are regulated, introducing new insights into pericyte biology, and building a path towards new therapeutic drug targets for treating cardiovascular disease and stroke.


2019 Research Grants

Jocelyn Beard Moran Memorial Fellowship
AWRP 2018 AHA Institutional Research Enhancement Award (AIREA)

Elena Galkin, PhD                     

Eastern Virginia Medical School
Norfolk, VA

Modified LDL uptake, B cell receptor signaling, and atherosclerosis:

Atherosclerosis is the leading cause of cardiovascular disease, the leading cause of death in the US.  B cells are a type of white blood cell in the body responsible for making antibodies, which are blood proteins produced in response to counteracting a specific foreign substance in the blood.  Though much is known about the general role of B cells in atherosclerosis, very little is known specifically how B cell receptor signaling affects B cell functions within atherosclerosis. Specifically, understanding how lipid uptake occurs in mobile white cells, also called macrophages, we can demonstrate how this process is critical in the development of atherosclerosis. Through better understanding the role of B cell function, our work will help to change existing models, with goals of uncovering new potential therapeutic targets of atherosclerosis.


Donna Gaff Marriott Award
Summer 2018 Predoctoral Fellowship

Federick Zasadny, BSE MS

George Washington University
Washington, DC

Rapid spectral mapping of ventricular absorbance to quantify homeostatic energetics in failing hearts:

Our research seeks to better understand energy distribution and demand process across a heart.   By directly quantifying the changes when heart rate is increased, we can begin to better understand how the energy supply and demand processes in the heart are synchronized. The ultimate goal is to understand the process in damaged hearts in patients with heart failure.   During the last five years, imaging technologies used on satellites in space have been miniaturized and made affordable by advances in nanofabrication. Our research seeks to harness these advances to image hearts with failing tissue and understand how the heart distributes energy when it is required to work harder.  This will allow clinicians to better understand how the heart responds under high workloads, such as during exercise. This is an important development that will possibly replace current diagnostic assumptions that do not look at energy modulation as a major therapeutic area in heart failure.

Anne Davis Camalier Award
2018 Transformational Project Award

Giulio Agnetti, PhD

Johns Hopkins University of Medicine
Baltimore, MD

Novel Mechanisms and Therapies for Proteopathic Heart Failure:

Despite the fact that Heart Failure (HF) represents a major cause of morbidity and mortality in Westernized countries, the molecular reasons underlying the decrease in the function of the heart with the progression of the disease are still unclear to date. There is an emerging consensus that the cause for the organ failure could be the formation of toxic substances, known as misshapen proteins. Misshapen proteins can have a tendency to group and rearrange to form toxic structures, which can cause tissue damage.   Currently, the identity of the misshapen protein in the heart is not known. We generated evidence that the protein “desmin” is prone to become misshapen in the heart, and we will study the toxic effect of this change over time as well as potential novel therapy.  The discovery of a mechanism that is independent of genetic mutations would allow the creation of different targeted diagnostics and treatments that could help prevent and cure HF.

Maggie Wimsatt Memorial Award

Patrick Calhoun, BS

VT Carilion Research Institute
Virginia Polytech Institute

Heart disease has been the leading cause of death in the United States for over 100 years. An important aspect of all forms of heart disease is a loss of proper cell-to-cell communication. The mechanism by which a virus disrupts this communication may be the same mechanism by which normal healthy hearts become diseased. Specifically, we will study a virus that infects human hearts and is capable of altering cell-to-cell communication. By controlling the cell-to-cell communication in a laboratory setting, we can assess how the virus may impact this process, as well as better understand similar dynamics in the absence of a viral infection. Understanding this mechanism will allow for therapeutic intervention and hopefully will significantly relieve the burden of cardiovascular disease.


2017 Grant Recipients


Honoring the former First Lady’s 25 years of devoted service to the Women’s Board

Matthew Barberio

Children’s Research Institute
Washington, DC

AWRP Winter 2017 Postdoctoral Fellowship

Our research addresses a potential mechanism by which youth obesity results in early-onset atherosclerotic development, a major risk factor for CVD and stroke. The studies are designed to understand the role of adipocyte-derived exosomes (specialized vesicles that are derived from fat cells) as well as the role of exosomal microRNA on suppressing cholesterol efflux gene expression. While the atherosclerotic cardiovascular disease is the leading cause of adult mortality, sub-clinical atherosclerosis is detectable in obese youth. Thus, understanding these processes in youth may help identify at-risk individuals. Identifying a novel mechanism and a biomarker for early detection will result in the foundation for primary prevention and treatment of CVD risk and allow children to live longer, healthier lives.


Honoring the founder of the Women’s Board


Che-Ying Kuo

University of Maryland
College Park, MD

AWRP Winter 2017 Predoctoral Fellowship

The purpose of our research is to investigate the mechanisms regulating the pathology of preeclampsia (PE), the elevated blood pressure during pregnancy. PE is the leading cause of maternal and perinatal morbidity and mortality affecting 3 to 8% of all pregnancies and it has been linked to increased risk of developing heart disease later in life for the mothers. In addition, recent research suggests that babies develop coronary heart disease, hypertension, and type 2 diabetes, originate from intrauterine growth restriction in which is caused by preeclampsia. We would like to understand ask are how does epidermal growth factor (EGF) regulate the development of preeclampsia. Despite the efforts to better understand the pathogenesis of preeclampsia, no effective treatment is available today other than early delivery of the fetus and placenta prematurely. In addition, there’s a lack of effective clinically relevant early predictor for preeclampsia, which will improve disease management.


Honoring many years of service to the Women’s Board

Linhao Ruan

Ruan Linhao

Johns Hopkins University School of Medicine
Baltimore, MD

AWRP WINTER 2017 Predoctoral Fellowship

Heart failure is common, costly, fatal and disabling. Current treatment options improve symptoms and prolong life, but do not address the fundamental problem of the loss of functional heart muscle. Although studies have been done to assess whether injecting regenerative (stem) cells into the heart improves heart function, none have been shown conclusively to be effective. Our research involved a way to print heart muscle using a special 3D printer, that uses heart cells (made from patient’s stem cells) and other supporting cells. We have studied 3D printed heart patches and their structural and functional properties. This proposal seeks to optimize the structural and functional properties of these tissues, in an effort to create cardiac disease models and reagents for myocardial repair. This is essential to the ultimate development of the use of stem cells in cardiac repair and identifying new therapeutic targets.



Honoring steadfast commitment to the Women’s Board 

Michael Schar

Johns Hopkins University School of Medicine
Baltimore, MD

AWRP WINTER 2017 Scientist Development Grant

Endothelial dysfunction occurs when blood vessels are not able to increase the size to meet demands for stress with increased blood flow. This dysfunction predicts future bad events such as cardiac infarction or stroke. To measure endothelial function, a “barometer” of vascular health, in arteries of the heart patients traditionally had to undergo an invasive catheterization procedure where a tube is put into the vessel to deliver X-ray visible dye into the heart. Our research introduces a noninvasive technique to measure the vessel size using magnetic resonance imaging (MRI). The goal of our research is to make the noninvasive MRI technique to measure vessel size more robust and tolerable for more patients and will then allow testing, without invasive catheterization, whether the vessels are healthy and whether their health improves after taking new medications or after lifestyle changes.



Katherine Owsiany

University of Virginia
Charlottesville, VA

AWRP WINTER 2017 Clinical Health Profession Student Training Program

It is thought that the response of immune cells and muscle cells might be the key factor that determines if the arterial damage is repaired or left vulnerable. Inflammation has been recognized as a key factor that drives arterial damage. Muscle cells were thought to help heal the damage, but our lab has recently discovered that the muscle cells can be inflammatory and might cause damage as well. Our research will focus on whether muscle cells can make a protein that is a signal to activate the negative effects of immune and muscle cells, called MCP1. The clinical trials and dose of a drug that blocks MCP1 were designed to target immune cells, but efforts were abandoned almost ten years ago after modest results. The key question in light of the current knowledge in the field is to determine if muscle cells are able to act like immune cells enough to cause arterial damage, but not enough to be susceptible to the same drugs. The answer could provide extraordinary impact, not only by providing a route for innovative therapies but making existing therapy more effective.



Xi Lan

Johns Hopkins University School of Medicine
Baltimore, MD

AWRP 2017 WINTER Postdoctoral Fellowship

Intracerebral hemorrhage (ICH) is a type of stroke that occurs when a blood vessel bursts in the brain and can cause death or lifelong disability. A protein called soluble epoxide hydrolase (sEH) plays an important role in ICH. Our research evaluates the role of sEH and will determine whether sEH can become a new therapeutic target in the treatment of this type of stroke. The substance, TPPU, is a sEH inhibitor, which might become a promising candidate drug to treat ICH. We will investigate the effects and mechanisms of sEH inhibition in ICH, and develop new therapies of ICH. Our long-term goal is to find a drug or therapy that can be used to treat intracerebral hemorrhage-induced brain damage and help patients to heal faster and more completely. Investigating the role of sEH in ICH will help us to find a new therapeutic way.