WEDNESDAY, June 30 (HealthDay News) -- Research on both mice and frozen human heart tissue has turned up evidence that a key enzyme involved in fetal heart development may also help trigger the onset of a serious heart disease in adulthood.
Latest Heart News
Such enlargement can lead to heart failure. But the research team from the Stanford University School of Medicine, led by Dr. Ching-Pin Chang, an assistant professor of cardiovascular medicine, believe they may have found a new target that may one day help treat the problem -- an enzyme known as "Brg1."
The finding is reported in the July 1 issue of Nature.
The authors noted that when active in the fetal hearts of mice, this enzyme serves to properly control heart muscle cell growth and differentiation, a function that is normally supposed to subside with age.
However, they found that when Brg1 is abnormally re-activated in mice by adult cardiac stress, a cellular process gets underway that reignites the fetal genes that normally would remain silent in adult hearts, in turn prompting troublesome heart enlargement.
"When the Brg1 gene is deleted, the stressed adult mouse heart has only minimal pathological changes," Chang noted in a news release. "It does not have significant hypertrophy. Theres no fibrosis or scarring."
This convinced Chang and his colleagues that Brg1 may indeed play an important role in heart enlargement disease -- a notion that was further reinforced by work with human heart tissue that had been frozen by the Stanford Cardiovascular Genomics and Proteomics Tissue Bank.
Working with tissue taken from four heart patients who had experienced heart enlargement as well as samples from six healthy patients, the researchers found that activation of Brg1 was linked to the disease. In addition, the greater the enzyme's activity, the more severe the disease.
"We hope to develop a chemical inhibitor that can target Brg1 activity in hypertrophic hearts and treat this disease," said Chang.
Copyright © 2010 HealthDay. All rights reserved.
SOURCE: Nature, June 28, 2010, news release.