Key gene for regenerating cells after heart attack pinpointed
In a new study, 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 Medical Center, teaming up to study in mice how heart tissue regenerates, found that microRNAs and #65533; tiny strands that regulate gene expression and #65533; 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 number one hurdle in cardiovascular research and #65533; 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," Dr. Hesham Sadek, senior author of a study, said.
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.
In the latest investigation, UTSW researchers found that hearts of young rodents mounted a robust regenerative response following myocardial infarction, but this restorative activity only occurs during the first week of life.
They then discovered that a microRNA called miR-15 disables the regenerative capacity after one week, but when miR-15 is blocked, the regenerative process can be sustained much longer.
"It is a fresh perspective on an age-old problem," Dr. Olson said.
"We're encouraged by this initial finding because it provides us with a therapeutic opportunity to manipulate the heart's regenerative potential," Olson added.
The study has been published in Proceedings of the National Academy of Sciences.