NORA ECCLES HARRISON
CARDIOVASCULAR RESEARCH &
TRAINING INSTITUTE

ADVANCING CARDIOVASCULAR RESEARCH SINCE 1969

CUTTING EDGE CARDIOVASCULAR RESEARCH

Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI) delivers cutting-edge cell-to-bedside research and education of cardiovascular disease, which is one of the leading causes of death worldwide. At the CVRTI, we are both developing new insights into the biology of heart muscle cells, and developing novel therapeutics for patients with heart failure and cardiac arrhythmias such as sudden cardiac death.

Located at the University of Utah, the CVRTI nucleates a campus wide, multidisciplinary team of fourteen individual investigator laboratories who are both scientists and physician scientists. The research of the laboratories spans from basic muscle biology and channel electrophysiology to metabolism and genetics. Founded in 1969, the CVRTI is one of the oldest cardiovascular institutes in the country, and its research has already impacted clinical care from development of the first artificial heart, to the genetic basis of long QT arrhythmias, to using electricity to map heart dimensions for arrhythmia ablation, to myocardial recovery.

Nora Eccles Harrison Cardiovascular Research & Training Institute building

CVRTI Seminar Series

Thursday, October 2, 2025
12:00 PM – 1:00 PM MT

Nicola headshot

Resolving Cellular Senescence Heterogeneity
with Single-Cell and Spatial Transcriptomics

Nicola Neretti, PhD

Associate Professor of Biology
Associate Director of the Center on the Biology of Aging
Brown University


Join us in person only at
Eccles Health Sciences Education Building, EHSEB, Bldg. 575, Room 1700, 25 S. 2000 E. (Lunch Provided)

Latest Blog

When the beat of your heart gets out of sync, or encounters other electrical problems, there are an array of devices and procedures available to help keep your heart pumping right. Cardiac electrophysiology devices and techniques are used to treat and diagnose electrical-related problems with your heart. From pacemakers to electrocardiograms (EKG), health care providers can keep your heart healthy or identify potentially life-threatening problems using electrophysiology.

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research team

Latest Publications

<h3>Cardiac Bridging Integrator 1 gene Therapy Rescues ChronicNon-ischemic Heart Failure in Minipigs</h3>

Cardiac Bridging Integrator 1 gene Therapy Rescues ChronicNon-ischemic Heart Failure in Minipigs

A groundbreaking study published by the Hong Laboratory in NPJ Regenerative Medicine showcases the potential of gene therapy to reverse chronic heart failure. The Hong Lab used a large-animal model to demonstrate that a single low-dose intravenous injection of gene therapy targeting cardiac bridging integrator 1 (cBIN1), a protein critical for heart muscle cell structure and calcium handling, significantly improved heart function and survival in minipigs with non-ischemic heart failure. The therapy restored cardiac cell architecture, reduced fluid retention, and normalized heart performance, offering a promising new avenue for treating heart failure by directly repairing failing heart muscle at the cellular level. These findings support future clinical trials using cBIN1 gene therapy in human patients with heart failure.
Hong Labs, NPJ Regen Med , 2024
<h3>Functional and Structural Remodeling as Atrial Fibrillation Progresses in a Persistent Atrial Fibrillation Canine Model </h3>

Functional and Structural Remodeling as Atrial Fibrillation Progresses in a Persistent Atrial Fibrillation Canine Model 

A recent study published by the Ranjan Laboratory in JACC: Clinical Electrophysiology sheds light on the progressive functional and structural changes in the heart associated with sustained atrial fibrillation (AF). Using a large-animal model of persistent AF, researchers conducted serial electrophysiological studies and advanced MRI imaging to track changes over six months. They found that as AF progressed, regions of the left atrium developed fibrosis, which was associated with slower electrical conduction and more uniform propagation directions, conditions conducive to sustaining arrhythmias. Notably, these changes were not confined to fibrotic areas but occurred throughout the atria, suggesting a diffuse remodeling process. These findings highlight the complexity of treating persistent AF and emphasize the need for new therapeutic strategies beyond targeting localized fibrosis.
Ranjan Lab, JACC Clin Electrophysiol, 2025
<h3>A Truncated Isoform of Connexin43 Caps Actin to Organize Forward Delivery of Full-length Connexin43 </h3>

A Truncated Isoform of Connexin43 Caps Actin to Organize Forward Delivery of Full-length Connexin43 

The Shaw Laboratory published a study that reveals how a small protein they discovered now called GJA1-20k plays a crucial role in heart health by guiding proper delivery of the heart’s communication channels to areas of cell-cell contact. Each heartbeat, billions of individual heart muscle cells have to contract in synchrony, and it is these communication channels known as Cx43 that are responsible for maintaining near simultaneous contraction, allowing the heart to work as a single effective organ. Although GJA1-20k is a shortened version of Cx43 made from the same genetic instructions, it doesn’t form the channels itself. Instead, it reshapes the cell’s internal skeleton (actin) to build pathways that help transport full-sized Cx43 to the cell-cell contact sites. Without GJA1-20k, Cx43 can’t reach its destination, disrupting cell-to-cell communication and increasing the risk of electrical disturbances in the heart known as arrhythmias. This discovery not only uncovers a new function for GJA1-20k as an actin-capping protein but also opens doors for new therapies designed to prevent dangerous arrhythmias from occurring and also to eliminate them when they do occur.
Shaw Lab, J Cell Biol. 2025

CAREERS AT CVRTI

We’re Hiring!
Openings for graduate students, postdoctoral fellows, and laboratory staff at the CVRTI.

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