More than 800,000 Americans are expected to have a heart attack this year. While survival rates have improved, many patients still suffer from irreversible 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 therapies aimed not only at preventing further heart damage but also enabling actual healing of injured hearts—an advancement not previously possible in medicine.
At UC San Diego, bioengineering professor Karen Christman has developed an injectable gel derived from extracellular matrix (ECM), a substance naturally produced by the body. The ECM gel is designed to reduce inflammation and organize itself into structures that attract new cells needed for blood vessel formation after a heart attack. “That stimulates the heart to have less scar tissue and preserve more cardiac muscle,” Christman explained.
Christman’s clinical trial in 2019 showed that injecting ECM directly into the heart was safe and helped patients recover better mobility compared to those who did not receive the treatment. She now plans further trials to test if delivering ECM through a blood vessel could allow for quicker and less invasive administration.
Meanwhile, UCLA’s Arjun Deb has identified a molecule called ENPP1 that acts as a brake on energy production in damaged heart cells. By developing a compound that temporarily blocks ENPP1 after a heart attack, Deb’s team found that only 5 percent of treated mice developed heart failure compared with over half of untreated animals. The experimental drug is now being tested for safety in humans following FDA clearance.
“This research represents a radical departure from existing lines of investigation which have led to the current drugs,” said Deb. Most available medications slow down tissue decline but cannot reverse existing damage; Deb’s approach aims to do so. 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.”
In another effort, researchers are studying zebrafish—a species known for its ability to regenerate its own heart tissue—to see if similar genetic mechanisms could be activated in humans. Scientists found that while both species share related genes involved in early development, human versions do not reactivate after injury like those of zebrafish do. Using CRISPR technology, researchers are adjusting gene expression in human stem cell models with hopes of triggering regeneration similar to what occurs naturally in zebrafish.
These research projects rely heavily on funding from agencies like the National Institutes of Health (NIH). Proposed federal budget cuts had threatened such scientific work, but recent advocacy efforts—including UC’s Speak Up for Science campaign—helped maintain funding levels for NIH and other science agencies this year.
UC leaders encourage continued community engagement as future budgets are negotiated to ensure support for medical research continues.
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