UT Southwestern Medical Center researchers have pinpointed a molecular mechanism needed to unleash the heart's ability to regenerate, a critical step toward developing eventual therapies for damage suffered following a heart attack.
Cardiologists and molecular biologists at UT Southwestern, teaming up to study in mice how heart tissue regenerates, found that microRNAs - tiny strands that regulate gene expression - contribute to the heart's ability to regenerate up to one week after birth. Soon thereafter the heart loses the ability to regenerate. By determining the fundamental mechanisms that control the heart's natural regenerative on-off switch, researchers have begun to better understand the No. 1 hurdle in cardiovascular research - the inability of the heart to regenerate following injury.
"For the first time since we began studying how cells respond to a heart attack, we now believe it is possible to activate a program of endogenous regeneration," said Dr. Hesham Sadek, assistant professor of internal medicine in the division of cardiology, and the senior author of a study in the Proceedings of the National Academy of Sciences.
Each year, nearly 1 million people in the United States have a heart attack, while about 600,000 die of cardiovascular disease annually. Heart disease is the leading cause of death in both men and women, according to figures from the Centers for Disease Control and Prevention.
As researchers worldwide strive to find ways that help the human heart cope with myriad illnesses and injuries, scientists at UT Southwestern have focused their attention on the heart's regenerative capabilities. In 2011, a team led by Dr. Eric Olson, chairman of molecular biology, and Dr. Sadek demonstrated that within three weeks of removing 15 percent of the newborn mouse heart, the organ was able to completely grow back the lost tissue, and as a result looked and functioned normally.