CINCINNATI – 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 fibrosis, organ enlargement and preserved heart function 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 function,” 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 improve muscle function and stop disease is an exciting new direction.”
Heart disease is one of the leading killers of people in the United States, according to the U.S. Centers for Disease Control. And a growing number of adults who were treated for congenital heart malformations as children – many who essentially had their hearts reconstructed – face lifelong potential health complications as a result.
Adult congenital heart disease is a growing priority and area of scientific inquiry at Cincinnati Children’s. Clinicians and researchers at the medical center are developing new clinical and research strategies for adults who were pediatric heart patients. This includes looking for what so far are elusive…