Florida Heart Research Foundation Cardiovascular Doctoral Student Grant Program

Florida Heart Research Foundation Cardiovascular Doctoral Student Grant Program is sponsored by Florida Heart Research Foundation. Supports doctoral students at Florida International University and Florida State University for research studies related to cardiovascular health, including peripheral arterial disease and heart failure.

Current Research | Miami, FL | Florida Heart Research Foundation Get Your Stop Heart Disease Plate Now! Miami Heart Research Institute Florida Heart Research Foundation Get Your Stop Heart Disease Plate Now!

HEART DISEASE RESEARCH, RESEARCHERS, & BREAKING NEWS Heart Disease Research, Researchers & NEWS HEART DISEASE RESEARCH, RESEARCHERS, & BREAKING NEWS Building upon a tradition of over half a century of leadership in cardiovascular disease , the Miami Heart Research Institute has embarked upon an exciting and ambitious research agenda.

We recognize the overwhelming need for resources devoted to developing new and promising initiatives, as well as the emerging role of institutional collaboration.

Miami Heart Research Institute is actively pursuing research programs in stem cell research, cardiovascular genetics, innovations in congestive heart failure, cardiac care of the elderly, emerging imaging capabilities, stress reduction, heart disease in the Hispanic population, long-term follow-up after heart surgery, dietary prevention of heart disease and noninvasive cures for coronary heart disease.

In order to pursue such a vigorous program we’ve combined the efforts of our outstanding staff of skilled researchers with experts from the Mayo Clinic, Georgetown University, Mount Sinai, Florida International University and the University of Miami among others.

By combining these sophisticated efforts with our active programs of outreach, education and prevention, we are able to rapidly transmit scientific advancement into community service. The future of cardiac research is very bright and exciting, and at Miami Heart Research Institute, it is now!

Building upon a tradition of over half a century of leadership in cardiovascular disease , the Miami Heart Research Institute has embarked upon an exciting and ambitious research agenda. We recognize the overwhelming need for resources devoted to developing new and promising initiatives, as well as the emerging role of institutional collaboration.

We believe and envision that through research combined with education about the causes, risk factors and lifestyle options, heart disease can be stopped and even reversed. Research discoveries benefit all of humanity and educations promotes informed choices thereby improving outcomes and quality of life. Research is imperative for our future health while education and prevention are key to our health today.

Miami Heart Research Institute is actively pursuing research programs in stem cell research, cardiovascular genetics, innovations in congestive heart failure, direct cardiac screening efforts to improve the care in an at-risk adult cancer survivor, emerging imaging capabilities, stress reduction, dietary prevention of heart disease and noninvasive cures for coronary heart disease and much more.

In order to pursue such a vigorous program we’ve combined our efforts with skilled researchers and experts from the Mayo Clinic, Georgetown University, Mount Sinai, Florida International University, Florida Atlantic University and the University of Miami among others.

By combining these sophisticated efforts with our active programs of education and prevention, we are able to rapidly transmit scientific advancement into community service. The future of cardiac research is very bright and exciting, and at Miami Heart Research Institute, it is now!

Miami Heart Research Institute & Florida Heart Research Foundation's policy on F&A Costs (Facilities and Administrative Costs), formerly known as indirect costs and overhead, is that MHRI & FHRF do not reimburse administrative expenses of any kind for awarded grants or projects.

This has always been the policy of Miami Heart Research Institute, Florida Heart Research Foundation and its Board, as well as part of every grant agreement we enter into. Miami Heart Research Institute and Florida Heart Research Foundation request that every grant be exclusively used to support an approved grant or project and pay for direct expenses of said approved grant or project.

No portion of the funds awarded for the approved grant or project will be used to pay indirect overhead expenses. 2026-2027 NEW & CONTINUED RESEARCH GRANT RECIPIENTS/PROJECTS: Mount Sinai Medical Center, research study entitled: "Whole Body Periodic Acceleration (pGz) in Heart Failure". Heart failure (HF) is a serious and increasingly common condition, particularly in older adults.

More than 50 out of every 1,000 people over the age of 65 are affected, and the lifetime risk of developing HF between ages 45 and 95 is as high as 20–45%. Individuals with HF often experience shortness of breath, fatigue, reduced ability to exercise, and fluid buildup in the lungs and body. Common causes include damage to the heart from prior heart attacks, as well as conditions such as diabetes and high blood pressure.

Despite advances in treatment, approximately half of patients diagnosed with HF die within five years. HF also leads to more than one million hospitalizations each year in the United States and costs over $30 billion annually, making it a major public health and economic challenge.

Whole Body Periodic Acceleration (pGz) is a non-invasive therapy that gently moves the body back and forth in a head-to-foot direction using a bed-like platform, similar to the motion of rocking a baby carriage. This movement creates beneficial pulses throughout the blood vessels, stimulating the release of substances that improve blood flow and support heart health.

With prior support from the Miami Heart Research Institute and Florida Heart Research Foundation, our laboratory has shown that pGz can improve heart function after cardiac arrest. We have also demonstrated that using pGz before a cardiac event (a strategy known as “preconditioning”) enhances recovery and preserves heart function.

This project will examine whether pGz can improve heart function in established heart failure, particularly in models that reflect the most common causes of the disease. We will also investigate how pGz works specifically whether it reduces heart scarring, inflammation, and harmful biological processes.

If successful, this research could lead to a simple, non-invasive therapy that improves survival, enhances quality of life, and reduces healthcare costs for patients living with heart failure. Georgetown University, research study entitled: “Restoration of Heart Function by Targeting Remodeling Pathways in the Ischemic and Stressed Heart”.

Cardiovascular disease remains the #1 cause of death in the US, despite remarkable advances in treatment and prevention, and heart failure affects more than 6 million Americans. Our laboratory is studying how chronic stress and inflammation lead to development of heart failure.

Heart failure is not only lethal, but it also greatly reduces quality of life, leads to shortness of breath, reduced exercise capacity, and a high risk of cardiac rhythm disturbances. Heart failure has many causes, but cures are lacking, and in most cases, treatment is focused on symptom relief.

Groundbreaking research in our laboratory, with the support of the MHRI, has now begun to shine light on exactly what goes wrong at the molecular and cellular level in some common forms of heart failure, leading the way to more effective treatment and reversal of this debilitating, progressive and lethal condition.

The heart is a pump made up of specialized muscle cells, called cardiac myocytes, that beat in coordination to circulate the blood. These cells are very long-lived, possibly more than 50 years, and are replaced very slowly (0. 5-1% per year).

Over a lifetime of continuous beating, they adapt remarkably to a range of physical and mental challenges. However, many common chronic diseases, such as high blood pressure, obesity and diabetes, generate stress that triggers inflammation, leads to abnormal function and cell death, and damages heart function. Aging by itself is an important contributor to both inflammation and cardiac damage.

Our project in the lab this year is to understand how age and inflammation affect the function and survival of cardiac myocytes in the context of chronic stress. We hypothesize that chronic inflammation associated with aging and age-related disorders is responsible for damage and dysfunction of cardiac myocytes and ultimately leads to heart failure.

We also hypothesize that the stress pathways we have identified and will further characterize in this year’s work will become practical targets for treatment with new types of specially-designed drugs from our collaborators at the University of Michigan. We will continue to explore the role of molecular pathways common to inflammation, cancer chemotherapy and aging through the use of genetically modified cells and animal models.

We will specifically explore the effect of RAGE, a receptor for inflammatory signals, and p300, a key regulator of the heart’s response to damage, on the immune cells that control cardiac inflammation and healing. Our ultimate goal is to prevent and reverse the morbidity and mortality of age- and stress-associated heart failure.

Florida Heart Research Foundation Cardiovascular Summer Research Internship Program at FIU: The Florida Heart Research Foundation Cardiovascular Summer Research Internship (CV-SRI) at Florida International University provides a transformative summer research experience for highly motivated high school students, incoming FIU undergraduates, and transfer students interested in cardiovascular and biomedical research.

Through this immersive eight-week program, participants are paired with FIU faculty mentors conducting cutting-edge cardiovascular related research. Students gain hands-on laboratory experience while developing critical thinking, scientific communication, and professional skills essential for success in STEM careers and advanced education.

The Foundation’s continued support has also allowed FIU to expand long-term undergraduate cardiovascular research opportunities through the Florida Heart Research Scholars program and the Florida Heart Undergraduate Research Fellowship.

These programs provide sustained faculty mentorship, advanced research training, and ongoing professional development for undergraduate students pursuing careers in medicine, biomedical science, and related health professions. Students regularly present their research at institutional, state, and national conferences, strengthening their preparation for graduate school, medical school, and research careers.

Together, these initiatives create a comprehensive research pathway that supports students from early exposure to advanced undergraduate research engagement.

The partnership between the Florida Heart Research Foundation and Florida International University continues to foster innovation, discovery, and educational opportunity while helping cultivate the next generation of cardiovascular researchers, healthcare professionals, and scientific leaders.

Florida Heart Research Foundation Cardiovascular Doctoral Student Grant Program at FIU: Aasma Dahal, PhD Candidate, Florida International University, research study entitled: “Peripheral Arterial Disease Monitoring: Spatio-Temporal Near-Infrared Spectroscopy Imaging in Pre-Clinical and Clinical Studies” .

Peripheral Arterial Disease (PAD) is a serious condition caused by narrowed blood vessels, often due to calcium buildup, leading to reduced blood flow and potential amputation. Millions of people worldwide live with PAD, and it significantly lowers the quality of life. One of the major causes of PAD is the calcium buildup within the blood vessels, which makes the blood vessels stiff and less flexible, restricting healthy blood flow.

Therefore, finding PAD early is important because treatment works best in early stages. However, many current diagnostic techniques like ultrasounds and angiograms are difficult to access in low-income communities and often fail to detect disease early. Some of these tests are also uncomfortable and involve harmful radiation, making them unsuitable for frequent monitoring of disease progression.

To address this challenge, our team has developed a new tool called “Near-Infrared Optical Scanner (NIROS)”. NIROS is a portable, safe device that does require direct contact to the skin to detect the disease. It uses harmless near-infrared light to measure blood flow and oxygenation in the feet.

Since PAD affects circulation, these measurements can reveal early signs of disease and track how it progresses over time. Our prior studies have shown that NIROS could detect abnormalities linked to calcification in mice heart by measuring blood flow changes in the tail. We now want to further evaluate it to determine whether it can detect the PAD-related changes in blood flow and oxygen.

This project has the potential to transform how PAD is detected and managed. NIROS offers earlier diagnosis, simpler follow-up, personalized care, ultimately improving the quality of life for those with PAD. This technique has a potential to be a portable, triage technique for a quick assessment of blood flow and oxygenation in the legs in emergency rooms procedures.

Katherine Kaiser, PhD Candidate, Florida International University, research study entitled: "Defining the Role of Caveolin-1 Localization in Tissue-Specific Calcification Mechanisms”. Calcium mineral formation is essential for building strong, healthy bones, but when calcium builds up inside blood vessels it can become dangerous and increase the risk of heart disease.

Although both bone and blood vessels can accumulate calcium mineral, this project explores the idea that these tissues use fundamentally different cellular mechanisms to control mineral formation. This research focuses on a protein called caveolin-1 (CAV1), which appears to play opposite roles in the mineral formation of bone cells and vascular cells.

Using advanced methods to study cell membranes, proteins, and signaling pathways, this project will investigate how the location of CAV1 within cells and its interaction with another signaling protein called ERK can influence how calcium minerals form.

By improving our understanding of how mineralization differs between bone and blood vessels, this work aims to help identify new strategies to prevent harmful vascular calcification while preserving the healthy mineralization needed for strong bones.

Perony Nogueira, PhD Candidate, Florida International University, research study entitled: "Developmental origin of elastin producing cells and mechanism underlying elastogenesis in the murine aortic valve". Every day, your heart's aortic valve opens and closes about 100,000 times, a tireless doorway between the heart's main chamber and the artery that carries oxygen to your entire body.

To survive that endless motion without tearing, this valve is woven with elastin, a stretchy protein that acts like the heart's built-in rubber bands. When elastin fails, valves stiffen or leak, and in rare genetic conditions like Williams-Beuren Syndrome and Supravalvular Aortic Stenosis, children are born without enough of it, leaving their major heart vessels dangerously narrowed from the very start of life.

Surprisingly, the same cells that color our skin and hair, also called melanocytes, also live inside the aortic valve. Their job there has long been mysterious. Both these pigment cells and many of the valve's structural cells share a common origin: a remarkable embryonic population called neural crest, which travels through the developing body to build tissues as different as facial bones, nerves, and skin pigment producing cells.

To test whether this lineage is responsible for the valve's elastin, we used genetically engineered mice in which the elastin gene was switched off only in neural crest cells. Our data showed that their valves contained significantly less elastin, identifying neural crest cells as major architects of these rubber bands.

When we studied albino mice, whose pigment pathway is broken, their valves had noticeably less elastin, as if the stage crew had walked off the job. When we treated these albino mice with L-DOPA, a small molecule already used safely in medicine for decades, the missing elastin came back.

This discovery opens a tangible door: repurposing a familiar, well-tolerated drug as a possible therapy to treat people with elastin-deficient valves, giving their hearts back the resilience they were never able to build on their own. Manuel Perez, PhD Candidate, Florida International University, research study entitled: "Flow-Induced Conditioning of Stem Cells for the Production of Cardioprotective Exosomes”.

Stem cells are especially important in biology because they have natural ways to protect themselves from stress and damage. One way they do this is by releasing special proteins that help keep them—and other cells—healthy. Interestingly, when gentle pressure or movement is applied to stem cells, they react by producing proteins that can help protect the heart.

These helpful proteins are packaged into tiny vesicles called exosomes. Exosomes act like messengers that travel between cells, carrying signals that promote healing. They have been shown to help heart cells survive, reduce damage, fight inflammation, and even help grow new blood vessels.

Our research is focused on finding ways to encourage stem cells to release more of these healing exosomes. We’re exploring how moving fluids, like the flow of blood, can “activate” the stem cells and cause them to produce more exosomes. This could be especially useful for repairing hearts damaged by blocked blood flow during a heart attack, a condition known as ischemia.

In our lab, we use a system that lets us control how the fluid flows over the stem cells. By adjusting the flow, we are identifying the ideal conditions that trigger the stem cells to release the most beneficial exosomes. If we can determine how to reliably produce these exosomes, we could create a new kind of treatment to help repair hearts damaged by disease.

Alexi Switz, PhD Candidate, Florida International University, research study entitled: “Development and Characterization of Helically Coiled Conductive Electrospun Fibers for Cardiac Patch Application”. Every 40 seconds, someone has a heart attack. Right now, the only approved way to fix the damage caused by a heart attack is through a heart transplant.

But since there aren’t enough donors and transplants can be risky, scientists are looking for other solutions. One idea is a cardiac patch—a kind of “living band-aid” that could repair the damaged heart. To make this patch, we are using a process called electrospinning to create two kinds of fibers.

The first type looks like rows of tiny Slinkys, and the second type looks like pencils stacked neatly in a case. The slinky-shaped fibers might help the patch bend and move with the beating of the heart. Conductive particles will also be added to the fibers, since the heart uses electrical signals to beat.

We plan to test how these fibers work, including how well they work with heart cells. The goal is to create a patch that could help heal heart damage in the future. Florida Heart Research Foundation Cardiovascular Doctoral Student Grant Program at FSU: Gallage Ariyaratne, PhD Candidate, Florida State University, research study entitled: "The Role of Non-Canonical NFkB Signaling in Arrhythmogenic Cardiomyopathy".

Arrhythmogenic Cardiomyopathy, or ACM, is an inherited form of heart disease that is a primary cause sudden cardiac death in young individuals. Presently, disease management focuses on symptomatic control using pharmacologic agents (e.g., antiarrhythmics) or invasive interventions, such as the placement of implantable cardioverter defibrillators (ICDs).

Sadly, these interventions do not target underlying mechanisms that contribute to chronic heart inflammation in patients with ACM, ultimately leading to heart failure. Recently, it has become more evident that these chronic inflammatory reactions are mediated by a protein (NFκB) that is often considered the “master regulator of inflammation.

” In cardiomyocytes (aka, heart cells) from patients with ACM, NFĸB is a major driver of inflammatory disease processes that contributes to disease progression in ACM. NFĸB triggers the release of pro-inflammatory mediators that drives local, heart inflammation, but also recruits immune effector cells (aka, white blood cells) like neutrophils and macrophages to the heart in large numbers.

These infiltrating immune cells can cause heart injury, cardiac dysfunction, and potentially lethal arrhythmias. Therefore, the objectives of this project are to elucidate the molecular and cellular mechanisms by which heart cells send signals to immune cells and influence their trafficking to the heart and induce myocardial inflammation.

By elucidating NFĸB-mediated pathways that cause heart inflammation, fibrosis, cardiac dysfunction and remodeling, and electrical instability, it may be possible to determine which disease processes are responsible for maintaining chronic heart inflammation.

As such, results from this project may uncover new pharmacologic targets – at the molecular level – that selectively block NFĸB-mediated signaling pathways, without suppressing the innate immune response. In summation, project outcomes aim to target the root causes of cardiomyocyte injury and shielding the heart from chronic inflammation that leads to heart failure.

Ronnie Chastain, PhD Candidate, Florida State University, research study entitled: "The Role of the C-domain of Troponin C in Health and Development of Cardiomyopathic Disease". Over the past decade, more evidence has accumulated implicating myofilament-related mechanisms in the progression of heart disease.

Investigating these mechanisms has uncovered different mutations or changes to sarcomere proteins, such as the troponin (Tn) complex of the thin filament or other proteins involved with myofilament function, that can lead to early developments in cardiac related-disease progression.

The Tn complex resides on the thin filament of sarcomeres, the functional unit of muscles, where it regulates the contractile ability of the muscle fiber in a Calcium (Ca2+)-dependent manner. Tn is comprised of three different proteins: TnI, TnT, and TnC.

TnC is the Ca2+-binding subunit of the complex and the cardiac (cTnC) isoform has three Ca2+-binding sites (II, III, IV); Ca2+ binding to site II (N-domain) ‘activates’ contraction whereas sites III and IV (C-domain) always have the divalentcations Mg2+ or Ca2+ bound.

My research will revolve around characterizing the mouse models that have mutations which block the ability of Ca2+ to bind the ‘structural binding sites’ of cTnC of the C-domain. After which, we will explore any biochemical or physical alterations to the myofilament to expand our understanding of the structural and modulatory elements involved in cardiac muscle regulation.

To investigate these possible changes, I will use various techniques such as skinned fiber mechanics, small-angle x-ray diffraction, echocardiogram and others to understand the different force- Ca2+ relationships, sarcomere alterations, and cardiac dysfunction in our models.

The information that can be garnered with this research will help increase our knowledge of cardiac muscle, which can lead to the resolution of better therapeutic targets or new modes of identification for early cardiac disease progression. Paula Nieto Morales, PhD Candidate, Florida State University, research study entitled: "Investigating the role of TNNC1 in Pediatric Dilated Cardiomyopathy".

Dilated cardiomyopathy (DCM) is the most common cardiomyopathy in children, with nearly 40% of symptomatic pediatric DCM (PDCM) cases resulting in heart transplantation or death within two years. PDCM involves the enlargement and weakening of the heart muscle, leading to impaired systolic function and heart failure. While the disease's clinical severity is well recognized, its molecular mechanisms remain complex and poorly understood.

Most cases are idiopathic or familial, involving mutations in over 30 genes. Recently, a rare variant in TNNC1, which encodes cardiac troponin C (cTnC), has been linked to PDCM. Nevertheless, the specific pathophysiology underlying this variant has yet to be fully elucidated.

Utilizing a newly developed mouse model, we characterized disease progression from the organ level down to the sarcomere, identifying a robust DCM phenotype as early as four weeks of age. Our findings highlight significant remodeling in myofilament calcium sensitivity and intracellular calcium handling.

A central focus of this study is the evaluation of a novel small-molecule myosin activator, currently in Phase II clinical trials for adults. Specifically, we will evaluate the in vivo effectiveness of this activator post β-adrenergic stimulation.

These in vivo assessments are paired with muscle mechanics studies using permeabilized fibers pre-treated with protein kinase A (to mimic β-adrenergic stimulation) to determine if the observed physiological benefits are achieved by directly correcting biophysical deficits at the myofilament level.

Although this molecule was designed to target thick-filament mutations, our research suggests that activating the thick-filament molecular motor can provide therapeutic benefit for cardiomyopathies caused by thin-filament defects. University of Miami, research study entitled: "The Use of CRISPR Interference (CRISPRi) Technology to Prevent Acute and Chronic Rejection in Organ Transplantation."

Organ transplantation using organs from the same species (allograft transplantation) remains the most effective treatment for patients with end-stage heart, lung, liver, and kidney diseases. Although advances in surgical techniques and immunosuppressive therapies have significantly improved patient outcomes, acute rejection (AR) and chronic rejection (CR) continue to be major causes of graft failure.

In heart transplantation, chronic rejection often manifests as cardiac allograft vasculopathy, a progressive narrowing of the coronary arteries that can ultimately lead to graft dysfunction and failure. To prevent rejection, transplant recipients must remain on lifelong immunosuppressive medications, which increase their risk of serious infections, malignancies, and other complications.

Therefore, developing strategies that reduce the immune response to transplanted organs while minimizing the need for long-term immunosuppression would provide substantial clinical benefits. With the continued support of the Miami Heart Research Institute (MHRI), Dr. Dong's laboratory has made significant progress toward addressing the root cause of transplant rejection—alloimmunity.

In previous funding cycles, the laboratory successfully utilized CRISPR-Cas9 genome-editing technology to suppress major histocompatibility complex (MHC) class I and class II molecules, the primary triggers of immune recognition and rejection.

Using a novel dual sgRNA approach, the team demonstrated efficient suppression of these molecules in endothelial cells and experimental transplantation models, resulting in reduced alloimmune responses and improved graft survival in mice. The laboratory subsequently extended this work to human leukocyte antigens (HLA), the human equivalent of MHC molecules, and successfully reduced HLA-ABC and HLA-DR expression in human cells.

Although CRISPR-Cas9 has proven to be a powerful and effective gene-editing tool, its reliance on permanent genomic modification presents potential challenges for clinical translation, including concerns regarding off-target effects and long-term safety.

To overcome these limitations, Dr. Dong's laboratory has transitioned to CRISPR interference (CRISPRi), an innovative gene-regulation technology that suppresses gene expression without altering the underlying DNA sequence.

CRISPRi utilizes a catalytically inactive (dead) Cas9 protein (dCas9) linked to a transcriptional repressor, allowing genes to be turned down in a reversible and highly controlled manner while preserving genomic integrity. The current project focuses on suppressing HLA Class I molecules (HLA-ABC), which play a critical role in activating immune responses against transplanted organs using CRISPRi.

The research team will use novel guide RNAs targeting the promoter regions of HLA-A, HLA-B, and HLA-C genes. Their preliminary studies showed substantial reduction of HLA-A both at transcription and protein levels, providing feasibility for the proposed approach.

Importantly, this suppression was achieved without permanently modifying the genome, representing a potentially safer and more clinically applicable approach than conventional gene editing. The laboratory is currently expanding this strategy to target HLA-B, HLA-C and HLA-DR, with the long-term goal of simultaneously suppressing both HLA Class I and Class II pathways that are major players in immune activation.

Successful completion of this work could significantly reduce the need for prolonged immunosuppressive therapy, decrease transplant-related complications, and transform the field of transplantation medicine. Ultimately, this technology may lead to the development of less immunogenic donor organs, reducing the need for lifelong immunosuppression and improving long-term transplant outcomes.

research study entitled: "Cardiolipin Remodeling as a Driver of Mitochondrial Dysfunction in Heart Failure with Preserved Ejection Fraction". Understanding and Treating Heart Failure with Preserved Ejection Fraction: Over 6 million Americans suffer from a form of heart failure called HFpEF (heart failure with preserved ejection fraction), where the heart becomes stiff and cannot relax properly between beats.

Despite being responsible for half of all heart failure cases, there are currently no effective treatments. Patients experience severe shortness of breath, fatigue, and have a life expectancy of only 5 years after diagnosis. Dr. Lina Shehadeh and her team at the Miami Heart Research Institute have discovered promising clues in animal models: the heart's energy-producing powerhouses—called mitochondria—appear to be damaged in HFpEF.

Specifically, the protective membranes surrounding these mitochondria become abnormal, potentially causing them to rupture and release toxic substances into the heart muscle. This damage may prevent the heart from generating enough energy to function properly. The research team identified a protein called Gasdermin D that may play a key role in this mitochondrial damage.

Their preliminary studies in mice suggest that when animals develop obesity, diabetes, or high cholesterol, Gasdermin D becomes overactive and creates holes in the mitochondria, potentially triggering a cascade of problems that leads to heart stiffness and failure. The exciting prospect: Gasdermin D can potentially be blocked by an FDA-approved drug called dimethyl fumarate (DMF), currently used to treat multiple sclerosis.

Because this drug has already been proven safe in humans for other conditions, it could potentially move to clinical testing faster than developing a completely new medication—if the animal studies prove successful. What the researchers will do: First, they will study mice with HFpEF to test the hypothesis that mitochondrial damage drives disease progression and determine whether DMF can prevent it.

Second, they will analyze blood samples from 273 heart failure patients to investigate whether simple blood tests might one day detect mitochondrial damage, potentially allowing doctors to diagnose the condition earlier and monitor treatment effectiveness. Third, they will test DMF in pigs, which have hearts very similar to humans, using the same advanced imaging and heart function tests used in patients.

These large animal studies are a critical step toward determining whether this approach could work in humans. Why this matters: This research represents an important step toward developing the first effective treatment for HFpEF. If the hypothesis proves correct in both mouse and pig models, it could pave the way for human clinical trials within 2-3 years—dramatically faster than typical drug development timelines.

Additionally, if the blood biomarkers under investigation prove useful, they could eventually help doctors identify which patients might benefit most from treatment, enabling personalized medicine approaches. Beyond HFpEF, this research may also provide insights for patients with diabetes-related heart disease and other conditions where mitochondrial damage appears to play a role.

This project offers hope for developing new treatments for millions of Americans living with a currently untreatable disease by testing whether an existing safe medication could be repurposed for HFpEF, based on promising findings from laboratory and animal models.

Roberta Lassance-Soares, PhD, University of South Florida, study entitled: "“Ischemic-Trained Extracellular Vesicles Reprogram Monocytes and Improve Hindlimb Ischemia Outcomes”. Critical limb ischemia (CLI) is a severe form of vascular disease in which the arteries supplying the leg become blocked, causing extreme pain, poor wound healing, and a high risk of amputation.

Many patients cannot undergo surgical procedures to restore blood flow, leaving them with very limited treatment options. New approaches that help the body naturally repair blood vessels are urgently needed to prevent limb loss and improve quality of life.

Our recent work shows that when blood flow is temporarily reduced in a controlled setting (a single ischemia insult), the body releases tiny particles into the bloodstream called extracellular vesicles (EVs). These EVs carry signals that “reprogram” immune cells, specifically monocytes, making them less inflammatory and able to better contribute to blood vessel growth.

This blood vessel growth, called neovascularization, is a natural process that improves blood flow in the limb. In this project, we will study whether EVs collected from mice subjected to an ischemia insult can reprogram monocytes in other mice, improving blood flow and healing after a limb blockage. First, we will determine whether these EVs change monocyte function inside the body.

Then, we will test whether giving these EVs to mice with poor circulation improves recovery and reduces tissue damage. By understanding how these EVs help blood