A vibrant exchange of scientific discovery and potential strategic collaboration took place February 23–24, 2026 at the University of Virginia, as researchers from AstraZeneca met with faculty from across the School of Medicine. 

The Robert M. Berne Cardiovascular Research Center and the Beirne B. Carter Center for Immunology Research hosted the two-day event, that brought together members of AstraZeneca’s Cardiovascular, Renal and Metabolism (CVRM) team, alongside its Respiratory & Immunology (R&I) team — including representatives from the company’s Open Innovation and Corporate Affairs teams— with UVA investigators and leadership from the School of Medicine (SOM) and the Office of the Vice President for Research (VPR). 

Strong Institutional Engagement 

The meetings reflected deep engagement on both sides. More than 60 UVA faculty laboratories submitted one-page proposals outlining innovative research programs and potential areas for collaboration with AstraZeneca. Following review, 33 labs were selected to present their science and participate in focused discussions about how future collaborations could be structured to accelerate discovery and therapeutic development. 

The breadth of science represented underscored UVA’s strengths across cardiovascular, renal, metabolic, respiratory, and immunologic research. Topics ranged from inflammatory drivers of cardiometabolic disease and immune-mediated tissue injury to biomarker discovery, advanced human model systems, translational data science, and novel therapeutic targets. 

UVA School of Medicine and Office of Research leadership were in attendance throughout the program, signaling institutional commitment to fostering high-impact academic–industry partnerships and supporting pathways that move discovery from bench to bedside. 

Science at the Interface of Disciplines 

A recurring theme of the meetings was the growing intersection between immune biology and cardiometabolic disease. Investigators from across the school of medicine highlighted advances in heart failure, vascular biology, thrombosis, and metabolic regulation. Other colleagues presented cutting-edge work in immune signaling, inflammation, host defense, and tissue homeostasis. 

AstraZeneca scientists engaged deeply with presenters, exploring how UVA’s mechanistic discoveries could align with the company’s global capabilities in drug development, translational medicine, and clinical trials. The presence of AstraZeneca’s Open Innovation Team created opportunities to discuss flexible partnership models, while Corporate Strategy leaders examined long-term alignment and portfolio integration. 

From Dialogue to Discovery 

The format emphasized interaction. Following each presentation, robust scientific discussion focused not only on experimental findings but also on practical next steps — from target validation and preclinical modeling to biomarker strategy and patient stratification. 

Networking sessions and smaller breakout meetings allowed faculty and AstraZeneca representatives to explore specific collaboration concepts in greater depth. Conversations centered on building sustainable connections designed to generate new discoveries and ultimately improve outcomes for patients worldwide. 

With strong participation, engaged institutional leadership, and cross-disciplinary scientific exchange, the February gathering marked an important milestone in strengthening ties between UVA and AstraZeneca. Participants left with a shared sense of momentum — and a commitment to advancing innovative science through collaboration in service of global patient care.

Link to Article on the UVA Research Website

Antonio Abbate, MD, PhD, a professor of medicine in the UVA Division of Cardiovascular Medicine, has been elected to the American Society for Clinical Investigation (ASCI), one of the nation’s most prestigious medical honor societies for physician-scientists.

Founded in 1908, the ASCI elects physician-scientists age 50 or younger in recognition of their significant research achievements and impact achieved. Its membership includes Nobel laureates, Lasker Award winners, and members of the National Academy of Medicine.

Dr. Abbatte will be formally inducted at the joint meeting of the ASCI, the Association of American Physicians, and the American Physician Scientists Association on April 17, 2026.

The ASCI is a nonprofit medical honor society composed of 3,500 physician-scientists across all medical specialties. Members are nominated and elected by their peers for having accomplished meritorious original, creative, and independent investigations in the clinical or allied sciences of medicine.

View the Article at the SOM Website

Hypertension, high blood pressure, affects approximately half of Americans over the age of 18. Persistent high blood pressure can contribute to heart attack, stroke, vision problems, and kidney disease, making it an important target for pharmaceutical development. “Many patients with high blood pressure are left with treatment-resistant hypertension,” says Araujo. ” There is a critical need to identify new ways of treating hypertension, and this requires a better understanding of pathological mechanisms.”

Blood pressure is controlled in part by smooth muscle cells inside our blood vessels, which can tighten or relax the vessel to control blood flow. “I am working on a fundamentally new mechanism for blood pressure regulation. This mechanism involves a well-known receptor called mineralocorticoid receptor, which alters ion channel activity and regulates smooth muscle contraction,” Araujo explains. To accomplish her objectives, she will use a combination of gene editing techniques, measurements of the electric currents inside cells, and super-resolution microscopy capable of observing individual proteins at the plasma membrane. Running these experiments in model systems and human samples with and without hypertension will allow Araujo to uncover new mechanisms of blood pressure regulation and possibly unlock new treatment options for hypertension.

The AHA Postdoctoral Fellowship is a prestigious, highly competitive award. “It’s an important milestone in my career, and I’m profoundly grateful for the training and support provided by the Sonkusare lab, as well as the research environment at the CVRC,” says Araujo.

In his lecture, Dr. Lindner discussed UVA’s role in developing and implementing contrast ultrasound, a technique where microbubbles are injected into a patient’s bloodstream to improve imaging in ultrasounds. “This is a UVA story,” explains Dr. Lindner. “Early first-in-human studies, safety and optimization research, and large clinical trials are all UVA work.” He also discussed how UVA continues to lead in the field by advancing new applications for contrast ultrasound and microbubbles. Dr. Lindner and other researchers are using the technology to deliver medications or genes to specific organs, diagnose disease with greater precision, and further improve the imaging potential of ultrasound methods.

Presenting to a lay audience presents unique challenges beyond making advanced science understandable to those without research experience. “You can often predict the questions a scientist will ask,” Dr. Lindner says. “Audiences who are less involved with day to day science will often ask unexpected, prescient questions that can really challenge you.” The Q & A period covered topics ranging from technology commercialization to safety considerations.

The U Ask, UVA Answers series continues February 8 with a presentation by Kelsey Johnson, PhD, from the Department of Astronomy.

The Weyman Award which is named for one of the early pioneers of cardiac imaging, generally receives 40-50 manuscripts from applicants. Only the top four are invited to compete and present at the ASE meeting ASE meeting. Dr. Morello presented his work in front of thousands of other scientists. “The ASE meeting lasts three days, and these presentations are its scientific highlight,” says Dr. Lindner. Dr. Morello joins 12 Weyman Award finalists mentored by Dr. Lindner in the past. “Dr. Morello joins a 20-year history of people from our lab receiving this award, which recognizes the best science in echocardiography,” Dr. Lindner explained. Receiving the award provides not only a monetary prize, but funding for travel to the European Society of Cardiovascular Imaging and the Japanese Society of Echocardiography meetings where Dr. Morello will present his work globally.

Dr. Morello’s presentation was titled “Cavitation-facilitated Augmentation of Myocyte Gene Delivery with Adeno-associated Vector-9: A Bioengineering Strategy to Address Clinical Gaps in Cardiac Gene Therapy.” In his talk, Dr. Morello described a new method for safely delivering gene therapies to tissue in the heart. Many gene therapies rely on using a modified virus, utilizing the virus’ natural ability to transfer DNA into cells to to correct a genetic flaw in the patient. This process is safe and effective in other organs, but the quantity of virus needed to treat genetic conditions in the heart exceeds safe level, a problem Dr. Lindner recognizes through his work as the Co-Chair of an NIH committee that oversees safety of gene and cell therapy trials. He and Dr. Morello have shown that  ultrasound-mediated vibration of microbubbles inside the heart blood vessels allows the virus to better penetrate into the heart’s tissues. More efficient viral delivery allowed Dr. Morello to lower the viral dose, resulting in a safe and effective treatment. He optimized the treatment conditions in mice before continuing his work at the Oregon National Primate Research Center. There, he showed that his methods were safe in non-human primates. He also showed that his methods are capable of partially reversing hypertrophic cardiomyopathy in mice that were developed by researchers in the CVRC.

The other research highlight of the ASE conference was the Brian Haluska Sonographer Research Award. The award recognizes sonographer-led research, where non-physicians are the study’s primary investigator. Gholson’s winning presentation, “Rapid Acceleration of Aortic Stenosis Progression in Echocardiography After Acute Coronary Syndrome,” went through the same vetting process as Dr. Morello’s, and involves a monetary award.

Gholson joined Dr. Lindner’s lab in 2022, becoming the team’s resident specialist in imaging the heart with ultrasound. Her research studied patients with progressive aortic stenosis, a condition that results in calcification of the heart valves over time. She studied over 15,000 records and images to build a database of patients with aortic stenosis. Gholson meticulously re-measured all the data points in her database and worked with collaborators to show that when one of these patients suffered a heart attack or similar cardiac event, the rate at which their valves thickened increased and did not return to the baseline rate of aortic stenosis progression for approximately two years. “Between collecting and re-analyzing all the data, I often left work cross-eyed to get what we needed,” joked Gholson.

Identifying cardiac stress events as the sole culprit for the increased rate of valve thickening was a statistical challenge. Gholson and collaborators were able to able to statistically prove that the increased rate of progressive valve thickening and restriction to opening was triggered by the heart attack. Other members of the laboratory are working on the molecular signals that get released after heart attack that are responsible for valve changes. Gholson is extending this research into other conditions to see whether damaging cardiac events accelerate disease progression. “This really is the tip of the iceberg,” she explained. “There are a lot of other conditions where we can make a difference in patient care.”

“The competition for both awards was incredibly fierce,” says Dr. Lindner. “This year had the highest quality science I’ve seen in both categories, so I’m extremely proud of Matteo and Bethany’s work.” Gholson credits the familial atmosphere at UVA for her success. “Recognition for this award really belongs to the entire research group. Our team shaped the project throughout, and I’m deeply grateful to Dr. Lindner, our collaborators, and our colleagues for their support, guidance, and partnership,” she stressed.

“Combining research and clinical training allows you to fundamentally advance our knowledge of human diseases,” Dr. Khetarpal explained. In his research, he studies the heart both as the primary organ of the circulatory system, but also as an important member of the endocrine system, regulating the body’s functions by releasing signaling molecules and hormones. These cardiac signals are modulated by exercise and illness. Natriuretic peptides, for example, are proteins released by the heart when it stretches or experiences increased pressure. They beneficially regulate blood pressure, and a common drug prescribed in heart failure, sacubitril-valsartan, in part prevents them from being broken down. “Since the discovery and targeting of natriuretic peptides for heart disease, we haven’t found many other heart-secreted proteins. I think there’s an opportunity to be inspired by this successful example and use new tools to identify other heart-derived proteins that can benefit patients,” says Dr. Khetarpal.

In his new paper, Dr. Khetarpal identifies a particular receptor in heart muscle cells, PGC-1α, essential for the heart to benefit from endurance exercise. Typically, exercise helps heart cells grow and function more efficiently. However, when Dr. Khetarpal deleted PGC-1α from those same cells, exercise no longer had any benefit. In fact, mice without PGC-1α suffered heart failure within 6 weeks of starting endurance training. With extensive work, Dr. Khetarpal showed that PGC-1α prevents the heart from releasing GDF15, a cardiac signaling molecule, and that a surplus of GDF15 led to the harmful consequences he observed. Further research will explore the roles of PGC-1α and GDF15 in heart failure and the heart’s ability to adapt to adapt to exercise. 

Dr. Khetarpal is particularly interested to join the cardiovascular research community at UVA. Six years ago, he interviewed with Dr. Gary Owens, director of the CVRC, when he was considering where to do his Fellowship training. The conversations he had during that time resonated strongly enough to draw him back for his independent career. “There is a widespread spirit of inclusivity, collaboration, and altruistic mentorship for young scientists in the Cardiology Division. It really makes me feel like this is the right place,” he said.

This support from UVA will be bolstered by the network provided by the NIH K08 and Burroughs Wellcome Fund awards, which both provide five years of funding for physician scientists transitioning from training into faculty positions. Dr. Khetarpal was one of only thirteen recipients of the Burroughs Wellcome Fund award this year. In addition to financial support, he will have access to intellectual resources in the form of guidance, mentorship, and collaboration with other award recipients. The Career Award for Medical Scientists funds all areas of medical research, facilitating contacts between researchers who might not otherwise interact.

Dr. Khetarpal’s research team is currently hiring at the postdoctoral, graduate/MSTP, and undergraduate academic levels.  His lab also has available research specialist positions. Individuals interested in joining the lab should contact Dr. Khetarpal via email, available on his lab website.

Blood vessels are made of concentric layers. Closest to the bloodstream is a layer of endothelial cells, which functions as an internal “skin”, separating flowing blood from the rest of the vessel. These cells become dysfunctional in obesity, contributing to a range of complications. Adjacent to this skin-like layer are smooth muscle cells, which control blood flow and pressure by contracting and relaxing. “When we think about inflammation, we typically focus on immune cells releasing inflammatory signals that affect endothelial or smooth muscle cells,” explains Sonkusare. “We asked a different question: ‘Can endothelial and smooth muscle cells themselves release inflammatory signals that elevate blood pressure?’”

Under healthy conditions, communication between the neighboring endothelial and smooth muscle cells helps maintain a normal blood pressure. Sonkusare’s team hypothesized that this cellular crosstalk becomes disrupted—or even harmful—in obesity. To study the cellular dynamics at play, the Sonkusare Lab fed mice a high-fat diet to develop obesity. They then isolated single cells from small blood vessels of these mice to analyze the inflammatory signals they released. Comparing these samples to those from mice fed a normal diet allowed the lab to identify obesity-dependent changes in inflammatory cell signaling. “We found that in obese mice, smooth muscle cells release the inflammatory molecule TNF, which acts on neighboring endothelial cells,” said Maniselvan Kuppusamy, PhD, first author of the study. Notably, this process occurs only in small arteries that regulate blood pressure—not in large arteries like the aorta. Importantly, the same increase in smooth muscle-derived TNF was observed in small arteries from obese human patients.                

The study further reveals that TNF from smooth muscle cells disrupts a calcium transport protein in endothelial cells, which in turn impairs the blood vessel’s ability to dilate, ultimately increasing blood pressure. Having identified this process, the team sought to disrupt it. The team started with two sets of genetically engineered mice: one set had smooth muscle cells incapable of producing TNF and another with endothelial cells unable to respond to TNF. In both cases, the obese mice showed improved vessel dilation and reduced blood pressure. The team then used a drug that blocks endothelial response to TNF, R7050, in obese mice without genetic modifications. R7050 successfully lowered their blood pressures. Finally, to confirm the clinical significance of their results, the Sonkusare Lab tested R7050 on blood vessels from UVA patients with and without obesity. The drug has beneficial effects in humans as well, opening new research avenues and potential therapies for patients with obesity-related hypertension.

The Sonkusare Lab is currently hiring at the Postdoctoral and Research Scientist levels. Interested parties should contact Sonkusare via email.

Walsh and his research team address a part of this question in their recent article, “Hematopoietic Loss of the Y Chromosome Activates Immune Checkpoints and Contributes to Impaired Senescent Cell Clearance and Renal Disease,” published in Science Translational Medicine. Having shown previously that LOY in immune cells leads to increased heart failure mortality, the team turned to other organs. The team, led by Yohei Arai, MD, PhD, a postdoctoral researcher in the Walsh lab, analyzed over 216,000 samples from the UK and determined that men with a high degree of Y chromosome loss were up to six times more likely to develop chronic kidney disease than those who had not lost their Y chromosomes. To understand why, Dr. Arai studied male mice with LOY. Like humans, these mice developed kidney failure as they aged and recovered poorly from kidney injuries, showing more scarring compared to their counterparts with an intact genome. “Interestingly, they also had more senescent cells—zombie-like cells that don’t grow, but secrete molecules that can promote tissue injury,” explains Walsh. When Dr. Arai treated the Y-less mice with drugs that target these zombie cells, the extra kidney damage the mice suffered from was reversed, suggesting that the senescent cells were an important part of the system.

Senescent cells are known to accumulate as we age because the body’s immune cells struggle to dispose of them as efficiently. It takes ten times longer for an old mouse to eliminate a senescent cell than a young mouse, for example. Dr. Arai suspected that male immune cells without Y chromosomes had a harder time eliminating these cells. His hypothesis was correct. When he compared immune cells with and without LOY, the ones with LOY were worse at destroying senescent cells. Looking deeper, Dr. Arai found that men and male mice who had lost their Y chromosomes send signals to immune cells that prevent them from killing dangerous cells. Blocking those signals restored normal function in both the kidneys and immune system.

Walsh and Dr. Arai hypothesize that LOY suppressing the immune system could explain why LOY is associated with a wide array of cancers in males—the body loses its ability to destroy tumors before they become established. Many tumors even use the same immune suppression molecules seen in this study to evade destruction, which could explain why men tend to respond better to cancer therapies that block those signals. Future work will continue to explore LOY, its consequences, and treatment options.