Mission to Personalize Heart Failure Care
Heart failure affects over seven million Americans and remains a leading cause of death among adults. At the University of Connecticut, researchers are charting a new course—personalized care based on a patient’s genetic profile.

“Unfortunately, heart failure treatment in the U.S. often follows a one-size-fits-all approach, which can be incomplete or ineffective,” says Dr. Travis Hinson, an NIH-funded cardiovascular physician-scientist jointly appointed at UConn Health and The Jackson Laboratory.
As UConn School of Medicine’s Pat and Jim Calhoun Endowed Professor, Hinson leads the Cardiovascular Genetics Program at UConn Health’s Calhoun Cardiology Center. His program bridges cutting-edge research from JAX to clinical applications, delivering tailored therapies to heart failure patients based on their unique genetic makeup.
Recreating the Patient’s Heart in the Lab
Before therapies ever reach a patient, they are rigorously tested in the lab using entirely-human engineered cardiac microtissues—miniature, beating heart models genetically matched to the individual. These are created from pluripotent stem cells, reprogrammed from the patient’s own blood or tissue and differentiated into spontaneously-beating heart cells.
This approach not only enables researchers to study the disease in a personalized model, but it also provides a powerful platform for therapeutic testing—a “clinical-trial-in-a-dish”—before moving into human subjects.

Tackling Dilated Cardiomyopathy with Precision
Hinson’s research focuses on dilated cardiomyopathy (DCM), the most common form of heart failure, affecting more than 1.75 million Americans. DCM causes the heart muscle to enlarge and weaken, often leading to life-threatening complications. Without intervention, half of patients diagnosed with DCM may die within five years.
Through his microtissue models, Hinson discovered that about 20 percent of DCM patients carry a gene variant that reduces the heart’s supply of titin, a key structural protein. This titin deficiency undermines the heart’s ability to pump efficiently—directly contributing to heart failure.
A CRISPR-Powered Breakthrough
Hinson’s lab has pioneered a CRISPR-based gene therapy to restore titin levels. By using adeno-associated viruses (AAVs) to deliver a gene activator, the therapy reactivates titin production directly in heart cells.
“We’re fortunate to be in the golden era of CRISPR,” Hinson says. “Our approach restores titin levels by 25 percent or more and halts disease progression.”
His team has demonstrated success in both mouse models and human heart organoids, with ambitious plans to launch first-in-human clinical trials within 5 years.
Looking Ahead
“This therapy addresses a critical unmet need in cardiovascular medicine,” says Hinson.
His groundbreaking work is supported by the NIH, the American Heart Association, and UConn Health and The Jackson Laboratory.
Recently, Hinson was among UConn Health faculty to showcase high-impact innovations at the inaugural Innovation Catalyst event, aimed at attracting commercialization partners. “The discoveries and translational research happening at UConn Health are truly amazing,” remarked Dr. Bruce T. Liang, dean of UConn School of Medicine.

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