More than 800,000 Americans are expected to experience a heart attack this year. While most will survive, many will face permanent damage to their heart muscle. “Many tissues in your body, such as the skin or the liver, can multiply and grow back. But the heart muscle is unable to do that,” said UCLA cardiologist and professor Arjun Deb. “When your heart muscle dies, you lose that muscle forever.”
Researchers at University of California campuses are working on new treatments aimed at helping damaged hearts heal, not just preventing further harm.
At UC San Diego, bioengineering professor Karen Christman has developed an injectable gel made from extracellular matrix (ECM), a substance naturally produced by the body. This gel is designed to reduce inflammation and promote new cell growth after a heart attack. According to Christman, “That stimulates the heart to have less scar tissue and preserve more cardiac muscle.” In a 2019 clinical trial, patients who received ECM injections were able to walk faster than those who did not receive the treatment, suggesting improved heart function. Christman is now preparing for another clinical trial that will test if ECM can be delivered through a blood vessel feeding the heart, potentially allowing for earlier and less invasive administration.
UCLA’s Arjun Deb has identified a molecule called ENPP1 that acts as a brake on energy production in damaged heart cells. Deb’s team developed a drug that temporarily blocks ENPP1, giving cells more energy to heal after injury. In animal studies following simulated heart attacks, only 5 percent of treated mice developed heart failure compared with over 50 percent of untreated mice. The drug is currently being tested in humans in a phase 1 clinical trial after receiving FDA clearance. “This research represents a radical departure from existing lines of investigation which have led to the current drugs,” said Deb. He added: “My team and I are enormously grateful to the NIH for believing in us and we hope to deliver soon to the American people a new therapy for heart disease.” This research has been funded entirely by state and federal agencies including the National Institutes of Health.
Another approach comes from studying zebrafish, which can regenerate their hearts after injury—a capability humans lack despite sharing similar genes involved in early development. Researchers led by Martik are using CRISPR technology on human stem cell models to modify gene expression so it resembles that of zebrafish with hopes of enabling human hearts to regrow tissue after damage. Martik estimates that therapies based on this work could become available within several years thanks in part to consistent support from the National Institutes of Health.
All three projects have relied heavily on federal funding from agencies like NIH. Recent proposals in Congress had threatened significant cuts to these science agencies’ budgets, which could have slowed progress and affected jobs and families across the country. Through advocacy efforts such as UC’s Speak Up for Science campaign—which encouraged community members to contact lawmakers—Congress ultimately passed a budget preserving bipartisan funding for NIH and other science agencies for another year.
The University of California continues its advocacy efforts as future federal budgets are debated, encouraging supporters to join its UC Advocacy Network or follow its Speak Up for Science campaign.
