{"id":235014,"date":"2025-09-11T07:15:50","date_gmt":"2025-09-11T11:15:50","guid":{"rendered":"https:\/\/today.uconn.edu\/?p=235014"},"modified":"2025-09-10T11:16:02","modified_gmt":"2025-09-10T15:16:02","slug":"correcting-a-deadly-error","status":"publish","type":"post","link":"https:\/\/today.uconn.edu\/2025\/09\/correcting-a-deadly-error\/","title":{"rendered":"Correcting a Deadly Error"},"content":{"rendered":"

Dr. Travis Hinson, a cardiovascular physician-scientist jointly appointed at UConn Health and The Jackson Laboratory (JAX), has been awarded $611,014 from the National Institutes of Health (NIH) to support his development of a therapy for a major cause of heart failure.<\/span>\u00a0<\/span><\/p>\n

As UConn School of Medicine\u2019s Pat and Jim Calhoun Endowed Professor, Hinson leads the Cardiovascular Genetics Program at UConn Health\u2019s Calhoun Cardiology Center<\/a>. His research focuses on understanding the causes and potential treatments for heart failure, a condition in which the heart is not pumping blood efficiently enough to provide oxygen to the body. <\/span>\u00a0<\/span><\/p>\n

One cause of heart failure is a disease known as dilated cardiomyopathy (DCM). In DCM, the muscles of the heart become enlarged and weakened, reducing their ability to pump blood effectively. The condition is quite serious; without intervention, half of patients diagnosed with DCM may die within five years.<\/span>\u00a0<\/span><\/p>\n

DCM\u00a0affects roughly one in 200 people, according to Hinson. Of these cases, between two and five percent can be attributed to a single genetic mutation, in a gene known as TNNT2.<\/span>\u00a0<\/span><\/p>\n

\u201cTNNT2 encodes a protein called troponin that affects how the cardiomyocyte [heart muscle cell] contracts in response to calcium,\u201d Hinson explains. <\/span>\u00a0<\/span><\/p>\n

In a normal heartbeat, calcium enters the cells of the heart muscles, signaling the muscles to contract. But when there is a misspelling in the TNNT2 mutation, heart cells do not respond in the same way, leading to DCM and eventually heart failure. As many as 100,000 Americans may have this mutation, according to Hinson.<\/span>\u00a0<\/span><\/p>\n

R<\/span>ight now, <\/span>we\u2019re<\/span> in<\/span> what I call the \u2018Dark Ages\u2019 of heart failure treatment.<\/span><\/p><\/blockquote>\n

\u201cThis is a big problem, and there aren\u2019t any treatments that really focus on the central mechanism,\u201d says Hinson. \u201cAll the drugs we have, they tend to have a lot of side effects, so they don\u2019t work for everyone \u2013\u00a0and they don\u2019t target the primary problem. Right now, we\u2019re kind of in what I call the \u2018Dark Ages\u2019 of heart failure treatment, where we don\u2019t really match up your treatment with your particular type of heart failure.\u201d<\/span>\u00a0<\/span><\/p>\n

Fortunately, Hinson\u2019s lab is dedicated to finding solutions for this and other causes of DCM. His work is at the cutting edge of personalized, precision medicine \u2013 understanding the root causes of an individual patient\u2019s heart condition and developing tailored treatments just for them.<\/span>\u00a0<\/span><\/p>\n

This work involves some innovative methods, like growing miniature, beating heart models<\/a> using a patient\u2019s own stem cells. Using these models, researchers can gain a better understanding of the patient\u2019s disease, as well as test the effectiveness of various therapies before administering them to the patient.<\/span>\u00a0<\/span><\/p>\n

Reaching the Heart of the Problem<\/h3>\n

In the case of the TNNT2 mutation, Hinson\u2019s in-development therapy uses an engineered type of virus known as an adeno-associated virus (AAV). It does what viruses do best: seek and enter host cells. But unlike a harmful virus, these AAVs are carrying helpful cargo. Once they enter heart cells, they deliver a drug that changes the way calcium stimulates the muscle contraction \u2013 getting things \u201cback to normal,\u201d says Hinson.<\/span><\/p>\n

\"Gloved
Dr. Hinson at his JAX laboratory holding petri dishes containing heart cells. He has pioneered a system to study the personalized genetics of a patient\u2019s heart failure by recreating beating heart tissue models using their own cells. (Peter Morenus\/UConn Photo)<\/figcaption><\/figure>\n

The results could be revolutionary.<\/span>\u00a0<\/span><\/p>\n

\u201cIt\u2019s a one-and-done, single-injection virus that delivers the drug into your heart, and then it targets the troponin piece,\u201d Hinson says. \u201cBasically, it changes out the abnormal, misspelled version for a normal version. This could be a good treatment for anyone who has a troponin T mutation.\u201d<\/span>\u00a0<\/span><\/p>\n

Funding for this project comes from the NIH Catalyze program, which helps move discoveries from the lab toward in-human trials.<\/span>\u00a0<\/span><\/p>\n

\u201cIt\u2019s a bridge from discovery in the lab towards a therapy in patients,\u201d Hinson says. \u201cThe NIH will help us navigate development of this therapy so that we can accelerate to humans as quickly as possible. To go from proof of concept to treating patients within five years \u2013 that’s the goal.\u201d<\/span>\u00a0<\/span><\/p>\n

A Unique Synergy<\/h3>\n

Hinson\u2019s innovative research group combines UConn Health\u2019s strengths in research and patient care with JAX\u2019s genomic medicine capabilities. He doesn\u2019t see these as separate spheres: treating patients helps usher in breakthroughs in the lab, and vice versa.<\/span>\u00a0<\/span><\/p>\n

\u201cI directly witness the impact on patients who have these disorders we want to fix,\u201d Hinson says. \u201cThis dual faculty role is a really supportive place for people like me. We need more positions like mine to help recruit people who do other pieces of the pie of genomic medicine … because it\u2019s such a big and important problem.\u201d<\/span>\u00a0<\/span><\/p>\n

Beyond just TNNT2, Hinson is also working on projects that target other mutations that lead to DCM or heart failure. He encourages potential academic and industry partners, or private funders who have been impacted by heart disease, to reach out if they are interested in supporting UConn Health\u2019s groundbreaking research in this area.<\/span>\u00a0<\/span><\/p>\n

“We have people in Connecticut who have these diseases — we need to be a leader in this area,\u201d Hinson says. \u201cIt brings in jobs, it brings in innovation, and it helps patients.\u201d<\/span>\u00a0<\/span><\/p>\n

 <\/p>\n

Hinson gratefully acknowledges UConn Health Ph.D. student Yu-Chieh Chen; postdoctoral associate Lisa Wren; and UConn genetic counselor Jennifer Stroop, all of whom have contributed vitally to the success of this TNNT2 treatment project.\u00a0<\/em><\/p>\n

Research reported in this publication was supported by the National Heart, Lung, And Blood Institute of the National Institutes of Health under Award Number R61HL181756. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.<\/span><\/i>\u00a0<\/span><\/p>\n","protected":false},"excerpt":{"rendered":"

NIH accelerating UConn Health cardiologist Dr. Travis Hinson\u2019s treatment for heart failure genetic mutation from lab toward in-human trials<\/p>\n","protected":false},"author":175,"featured_media":235015,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"_crdt_document":"","wds_primary_category":0,"wds_primary_series":0,"wds_primary_attribution":0,"footnotes":""},"categories":[1969,2460,2231,2256,2076,2235,179],"tags":[],"magazine-issues":[],"coauthors":[2413],"class_list":["post-235014","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-cardiology","category-faculty","category-health-well-being","category-innovation","category-research","category-today-homepage","category-uconn-health"],"pp_statuses_selecting_workflow":false,"pp_workflow_action":"current","pp_status_selection":"publish","acf":[],"publishpress_future_action":{"enabled":false,"date":"2026-05-11 14:02:21","action":"change-status","newStatus":"draft","terms":[],"taxonomy":"category","extraData":[]},"publishpress_future_workflow_manual_trigger":{"enabledWorkflows":[]},"_links":{"self":[{"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/posts\/235014","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/users\/175"}],"replies":[{"embeddable":true,"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/comments?post=235014"}],"version-history":[{"count":12,"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/posts\/235014\/revisions"}],"predecessor-version":[{"id":235157,"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/posts\/235014\/revisions\/235157"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/media\/235015"}],"wp:attachment":[{"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/media?parent=235014"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/categories?post=235014"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/tags?post=235014"},{"taxonomy":"magazine-issue","embeddable":true,"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/magazine-issues?post=235014"},{"taxonomy":"author","embeddable":true,"href":"https:\/\/today.uconn.edu\/wp-rest\/wp\/v2\/coauthors?post=235014"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}