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Your Environment. Your Health.

Potential Therapy for Stopping Cardiac Fibrosis Discovered

A unique therapy for preventing or reducing harmful cardiac scar tissue, a common development in people following a heart attack, may result from a new finding by NIEHS-supported researchers at the University of California, Davis (UC Davis). Their study of laboratory mice shows that blocking soluble epoxide hydrolase (sEH), an enzyme that promotes inflammation, can prevent cardiac fibrosis, a scarring tissue damage that often leads to heart failure.

UC Davis researchers Bruce Hammock, Ph.D., and Nipavan Chiamvimonvat, M.D. view computer screen

UC Davis researchers Bruce Hammock, Ph.D., and Nipavan Chiamvimonvat, M.D.
(Photo courtesy of Kathy Keatley Garvey)

A combined 11-scientist team determined that treatment with a potent sEH inhibitor results in significant improvement in cardiac function. They also determined the molecular mechanisms underlying this beneficial effect after a heart attack. The scientists were led by Bruce Hammock, Ph.D., who directs the UC Davis Superfund Research Program, and Nipavan Chiamvimonvat, M.D., a professor of cardiovascular medicine at UC Davis.

In the study, mice receiving sEH inhibitors showed significant decreases in adverse cardiac muscle remodeling, or enlargement, following a heart attack. Their overall cardiac function also improved. Additional tests performed in Hammock’s lab indicated significantly reduced levels of inflammatory factors in the mice. The research team hopes to next test the sEH inhibitor on another animal model as a precursor to conducting human clinical trials.

"Cardiac fibrosis is a common final pathway for many cardiac diseases and heart failure that has been difficult to treat in the clinic,” said Javier E. López , M.D., a cardiovascular medicine professor at UC Davis and part of the research team. “This study shines some light on to this pathway and offers perhaps a new therapeutic target that may expand available treatments for these patients in the future."

For more information, visit the UC Davis news webpage .

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