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New drug may block muscle scarring linked to heart failure

The experimental treatment works by targeting molecules on alpha V integrins, or scar-forming cells.

By Amy Wallace

Oct. 24 (UPI) -- Excessive scarring of the heart muscle can lead to heart failure, a potentially deadly condition with no cure, but a new drug may provide hope for patients.

Muscle scarring or fibrosis, including skeletal and cardiac muscle fibrosis, are major causes of morbidity and mortality worldwide, with no real treatment options.

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A study, published today in Nature Communications, tested the efficiacy of an experimental drug to prevent heart muscle scarring after a cardiovascular event, such as a heart attack. The experimental treatment works by targeting molecules on alpha V integrins, or scar-forming cells.

"Cardiac fibrosis is a major contributor to chronic heart failure, which is a major cause of death worldwide," Neil Henderson, of the Medical Research Council Center for Inflammation Research at the University of Edinburgh, said in a news release. "Our research has identified a promising therapeutic target in the development of new treatments for patients with chronic heart failure."

An earlier study by the University of North Carolina Chapel Hill found a method to reprogram scar tissue cells into healthy heart muscle cells.

UNC researchers identified two methods to regenerate cardiomyocytes, heart muscle cells that normally remain damaged following a heart attack.

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For the current study by the University of Edinburgh, researchers blocked the alpha V integrins molecules with an experimental drug.

"We found that Pdgfrb-Cre effectively targeted quiescent PDGFRβ+ cells and activated myofibroblasts in both skeletal and cardiac muscle," study authors wrote. "Selective depletion of αv integrins on PDGFRβ+ cells protected mice from fibrosis in both these muscle types, and αv integrin depletion on PDGFRβ+ cells had no adverse effects on skeletal muscle regeneration."

Researchers also found that treatment with a small molecule inhibitor of αv integrins, or CWHM 12, weakened fibrosis in both skeletal and heart muscle after the fibrotic process was established.

"Scarring of the heart muscle has a major impact on the heart's ability to pump effectively," said Jeremy Pearson, professor and associate medical director at the British Heart Foundation. "This can lead to heart failure and there is no effective treatment at the moment. By finding a new way to limit scarring in the hearts of mice, this research has unlocked the route to a potential treatment for this life-threatening problem."

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