June 5 (UPI) -- Researchers at Baylor College of Medicine have uncovered new insights into why heart muscle lacks the ability of self-repair, which may lead to more effective ways of treating heart disease.
Heart disease is the leading cause of death in the United States, according to the Centers for Disease Control and Prevention, due to the fact that the heart muscle is one of the least renewable tissues in the body.
A study by Baylor College of Medicine and the Texas Heart Institute revealed a previously unknown connection between processes that keeps the heart from repairing itself.
"We are investigating the question of why the heart muscle doesn't renew," Dr. James Martin, a professor and chair in Regenerative Medicine at Baylor College of Medicine, said in a press release. "In this study, we focused on two pathways of cardiomyocytes, or heart cells, the Hippo pathway, which is involved in stopping renewal of adult cardiomyocytes, and the dystrophin glycoprotein complex [DGC] pathway, essential for cardiomyocyte normal functions. We are also interested in studying mutations in DGC components because patients with these mutations have a muscle wasting disease called muscular dystrophy."
Researchers genetically engineered mice to lack genes involved in one or both pathways, then determined the ability of the heart to repair an injury showing for the first time that dystroglycan 1, a component of the DGC pathway, directly binds to Yap, a part of the Hippo pathway, to inhibit cardiomyocyte proliferation.
The findings could improve cardiac function in children with muscular dystrophy who often have severe reduction in cardiac function.
"The discovery that the Hippo and the DGC pathways connect in the cardiomyocyte and that together they act as 'brakes' or stop signals to cell proliferation opens the possibility that by disrupting this interaction one day it might be possible to help adult cardiomyocytes proliferate and heal injuries caused by a heart attack, for example," Martin said.
The study was published in Nature.
