Scientists test way to stop heart damage after cardiac injury

The microscopic image on left shows a control mouse heart cross section after simulated cardiac injury with significant fibrosis. The image the right shows the “experimental model” in which Wnt/b-catenin was inhibited in the hearts of mice, resulting in reduced fibrosis. Scientists report early research results in Nature Communications that suggest scientists might be on to a way to preserve cardiac function after heart attacks or for people with certain inherited heart defects. Credit: Cincinnati Children’s

Early research results suggest scientists might be on to a way to preserve heart function after heart attacks or for people with inherited heart defects called congenital cardiomyopathies.

Researchers at the Cincinnati Children’s Heart Institute report Sept. 28 in Nature Communications that after simulating heart injury in laboratory mouse models, they stopped or slowed cardiac , organ enlargement and preserved by blocking a well-known molecular pathway.

The Wnt/β-catenin signaling pathway is involved in several of the body’s fundamental biological processes. After heart injury, however, Wnt/β-catenin signaling ramps up in cardiac fibroblast cells to cause fibrosis, scarring and harmful enlargement of the heart muscle, according to the researchers.

“Our findings provide new insights on what causes cardiac fibrosis and they open the potential for finding new therapeutic approaches to fight it and preserve heart ,” says Katherine Yutzey, PhD, lead study author and scientist in Molecular Cardiovascular Biology. “Wnt/β-catenin signaling is involved in many normal and disease processes and it’s tough to target therapeutically. But the idea that early targeting of fibrotic response in cardiac disease may…

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