This injected protein-like polymer helps tissues heal after a heart attack
Peer-Reviewed Publication
In recognition of Heart Health Month, we’re spotlighting the importance of cardiovascular wellness. From risk factors and prevention to innovative treatments, we’re exploring the science and stories shaping heart health today.
Updates every hour. Last Updated: 26-Jul-2025 06:10 ET (26-Jul-2025 10:10 GMT/UTC)
Researchers have developed a new therapy that can be injected intravenously right after a heart attack to promote healing and prevent heart failure. The therapy both prompts the immune system to encourage tissue repair and promotes survival of heart muscle cells after a heart attack. Researchers tested the therapy in rats and showed that it is effective up to five weeks after injection.
Scientists at Northwestern University and University of California San Diego have developed a new, potent injectable therapy that can protect the heart from damage after a heart attack. After showing success in cell culture, the scientists tested their new therapy in a rat model of heart attack. Following a single, low-dose intravenous injection, the animals experienced decreased inflammation and cell death along with improved cardiac function and increased growth of new blood vessels.
Mount Sinai-led research can transform how hospitals triage, risk-stratify, and counsel patients to save lives
A pioneering Israeli study has identified TRIM63 as a significant genetic contributor to hypertrophic cardiomyopathy (HCM)—the most common hereditary heart disease worldwide. The findings, published in Circulation: Genomic and Precision Medicine, could transform genetic screening and treatment protocols for HCM patients around the globe.
Led by Dr. Noa Ruhrman Shahar of Rabin Medical Center (Beilinson Hospital) and Professor Shay Ben-Shachar of the Clalit Research Institute, the study provides compelling evidence for the gene’s role in both causing and increasing susceptibility to HCM.
“This is a life-saving discovery,” said Dr. Ruhrman Shahar. “Recognizing carriers of disease-causing TRIM63 mutations enables early monitoring and intervention, dramatically lowering the risk of severe, even fatal, cardiac events.”