Project Grant R01HL171989
- The National Heart Lung and Blood Institute awarded President and Fellows of Harvard College $151,040 on February 5, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to investigate the role of TOLLOID proteases in atrial fibrosis and atrial fibrillation pathogenesis. The research uses gene-edited mouse models, both with and without surgically induced atrial fibrosis, to examine how TOLLOID protease-mediated cleavage of Growth Differentiation Factor 11 (GDF11) regulates...
- The National Heart, Lung, and Blood Institute awarded Vanderbilt University Medical Center $1.732 million on June 1, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to develop ENT-verticilide, a selective ryanodine receptor type 2 (RYR2) inhibitor, as a novel antiarrhythmic drug for atrial fibrillation treatment. The research addresses the clinical challenge that current antiarrhythmic therapies fail frequently due to heterogeneity in underlying causes of atrial...
- The National Heart, Lung, and Blood Institute awarded the University of California, Los Angeles $169,776 on July 15, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to study molecular targets of postoperative atrial fibrillation. This Project Grant (K08HL179450) supports research identifying why atrial fibrillation develops after cardiac surgery—a complication affecting 30–40% of cardiac surgical patients—with focus on fibroblast growth factor 13 expression in atrial...
- The National Heart, Lung, and Blood Institute awarded The Leland Stanford Junior University $743,696 on July 1, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to investigate atrial fibrillation in patients with hematologic malignancies receiving Bruton's tyrosine kinase inhibitor therapy. The project prospectively characterizes the incidence and burden of atrial fibrillation in BTKi-treated patients, develops BTKi-specific atrial fibrillation risk scores, and identifies...
- The National Heart Lung and Blood Institute awarded Inomagen Therapeutics, Inc. $1,412,149 on September 1, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to advance IGN001, a non-viral short hairpin RNA plasmid designed to silence NOX2 and modify the disease substrate in atrial fibrillation without destroying atrial tissue. The recipient will conduct three aims: define the dose-dependent molecular activity and safety of IGN001 in healthy canines by assessing NOX2...
- The National Heart, Lung, and Blood Institute awarded the University of Massachusetts Medical School $858,456 on September 1, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837, Assistance Listing R01HL184047) to develop and test an interoperable shared decision-making tool integrated into electronic health records for stroke prevention in atrial fibrillation patients. The project, titled DECIDE-AF, addresses suboptimal anticoagulation initiation and persistence among AF...
- The National Heart, Lung, and Blood Institute awarded Cincinnati Children's Hospital Medical Center $498,000 on September 25, 2025, under the Cardiovascular Diseases Research program (CFDA 93.837) to investigate the role of the transcription factor PITX2 in epigenetic patterning of the left atrium in the context of atrial fibrillation. The award is a project grant with a period of performance through July 31, 2028, and place of performance in Cincinnati, Ohio. The research addresses the...
- Federal Project Grant Award Summary Duke University's Office of Research Administration received a $242,250 Project Grant from the National Heart, Lung, and Blood Institute (NHLBI) under the Cardiovascular Diseases Research program (CFDA 93.837), effective July 1, 2025 through June 30, 2027. This award funds research examining the relationship between atrial fibrillation (AF), oral anticoagulation therapy, and retinal stroke (central retinal artery occlusion) using an instrumental variable...
- The National Institutes of Health National Heart, Lung, and Blood Institute awarded the University of Arizona $743,545 on July 15, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to develop deep learning methods for drug discovery targeting atrial fibrillation. The research focuses on identifying selective inhibitors of small conductance calcium-activated potassium (SK) channels as a therapeutic approach to atrial fibrillation. The project builds on the investigative...
- The National Heart, Lung, and Blood Institute awarded the University of South Florida $2.186 million on September 19, 2025, under the Cardiovascular Diseases Research program (CFDA 93.837) to investigate the relationship between atrial microvascular and endothelial dysfunction and postoperative atrial fibrillation. The research evaluates microvascular signaling pathways responsible for myogenic, vasomotor, and endothelial dysfunction of the atrial microvasculature in patients with...
THERAPEUTIC MODULATION OF ATRIAL REMODELING - PROJECT SUMMARY ATRIAL FIBRILLATION (AF) IS A LEADING CAUSE OF STROKE AND A MAJOR CAUSE OF MORBIDITY AND MORTALITY IN THE US. AF IS HIGHLY ASSOCIATED WITH CONDITIONS THAT ELEVATE INTRACARDIAC PRESSURE, SUCH AS HYPERTENSION AND HEART FAILURE. CARDIAC PRESSURE OVERLOAD INDUCES ELECTRICAL AND STRUCTURAL CHANGES IN THE LEFT ATRIUM (LA) IN A PROCESS KNOWN AS ATRIAL REMODELING THAT CREATES THE SUBSTRATE FOR AF. THERE ARE CURRENTLY NO THERAPIES THAT DIRECTLY ADDRESS THE UNDERLYING ATRIAL REMODELING PROCESS. TO ADDRESS THIS CRITICAL UNMET NEED, WE FOCUSED ON SIGNALING PATHWAYS ESSENTIAL FOR ATRIAL DEVELOPMENT TO IDENTIFY NOVEL THERAPEUTIC TARGETS. WE FOUND THAT ALL-TRANS RETINOIC ACID (ATRA), A VITAMIN A DERIVATIVE THAT IS ESSENTIAL FOR ATRIAL DEVELOPMENT, CAN PREVENT AND REVERSE ATRIAL REMODELING IN A CARDIAC PRESSURE OVERLOAD MODEL. COMPARATIVE LEFT ATRIAL TRANSCRIPTOMIC ANALYSIS REVEALED THAT ATRA TREATMENT NORMALIZES IMPORTANT METABOLIC PATHWAYS, ATRIAL DEVELOPMENTAL PATHWAYS, RAPID CONDUCTION GENES, AND REDUCES PRO-INFLAMMATORY AND PRO-FIBROTIC PATHWAYS. SINGLE NUCLEAR SEQUENCING ANALYSIS SHOWS THAT ATRA CHANGES THE POPULATION OF MACROPHAGES FROM A PRO-INFLAMMATORY SUBTYPE TO A REPARATIVE SUBTYPE. ATRA CAN ALSO PROTECT AGAINST ATRIAL FIBROSIS IN A NON-PRESSURE OVERLOAD MOUSE MODEL OF AF. ATRA IS FDA APPROVED FOR THE TREATMENT OF ACUTE PROMYELOCYTIC LEUKEMIA (APL). WE FOUND THAT ATRA THERAPY IMPROVES ATRIAL CONDUCTION PARAMETERS IN APL PATIENTS AT ONE MONTH OF TREATMENT. OUR FINDINGS STRONGLY SUPPORT ATRA AS A POWERFUL NEW TREATMENT THAT CAN REVERSE ATRIAL REMODELING FOR THE PREVENTION OF AF.
Mod # | Description | ReasonForModification | Federal Obligation | Date |
|---|---|---|---|---|
| Not listed | $682.0k | 7/10/26 | ||
| Not listed | $695.9k | 5/30/25 | ||
| Not listed | $695.9k | 6/14/24 | ||
| Not listed | $695.9k | 6/14/24 |