APR 08, 2015 9:16 AM PDT

Turbo-Charging Hormone Can Regrow the Heart

WRITTEN BY: Judy O'Rourke
Researchers have discovered a way to stimulate muscle regrowth in the heart of a mouse, opening up prospects of new treatments for many who suffer heart attacks each year.

The animal study found it was possible to regenerate muscle cell numbers in the heart by up to 45 percent by ‘turbo-charging' a hormone that helped coordinate cell growth.

According to study lead author, associate professor Richard Harvey, PhD, UNSW, based at the Victor Chang Cardiac Research Institute, New South Wales, Australia, this is an important step toward repairing a broken heart.

"Unlike blood, hair, or skin cells, which can renew themselves throughout life, cell division in the heart virtually comes to a standstill shortly after birth, which means the heart can't fully regenerate if it is damaged later in life," Harvey says.

"Previous studies have demonstrated that it is possible to coax heart muscle cells to proliferate again, but only at very trivial levels," he says. "What the research team has been able to do is boost heart muscle cell numbers by as much as 45 percent after a heart attack."

The scientists focused on a signalling system in the heart driven by a hormone called ‘neuregulin'.

By switching the neuregulin pathway to ‘turbo charge', the researchers found that heart muscle cells continued to divide in a spectacular way in both the adolescent and adult periods. Stimulating the neuregulin pathway during a heart attack led to replacement of lost muscle.

"This big achievement will focus the attention of the field on heart muscle cell replacement as a therapeutic option for ischemic heart disease," Harvey says. "The dream is that one day we will be able to regenerate damaged heart tissue, much like a salamander can regrow a new limb if it is bitten off by a predator. Just imagine if the heart could learn to regrow and heal itself. That would be the ultimate prize."

The research, conducted at the Weizmann Institute of Science in collaboration with the Victor Chang Cardiac Research Institute, and titled "ERBB2 triggers mammalian heart regeneration by promoting cardiomyocyte dedifferentiation and proliferation," is published in Nature Cell Biology.

[Source: UNSW]
About the Author
  • Judy O'Rourke worked as a newspaper reporter before becoming chief editor of Clinical Lab Products magazine. As a freelance writer today, she is interested in finding the story behind the latest developments in medicine and science, and in learning what lies ahead.
You May Also Like
AUG 08, 2019
Cardiology
AUG 08, 2019
The Best Way to Test Blood Pressure and Find Heart Disease
Heart disease causes hundreds of thousands of deaths annually -- can a new study on blood pressure tests guide doctors toward earlier diagnosis? About one ...
AUG 14, 2019
Cardiology
AUG 14, 2019
Living Near Fast Food Increases Heart Attack Risk
A new study examines the relationship between heart attacks and fast food chain-proximity. Heart disease, including heart attacks, are one of the leading c...
OCT 18, 2019
Cardiology
OCT 18, 2019
Find the Motivation to Exercise with Imagery
Those involved in professional sports have a lot on their plate. From fitting in intense regular workouts to getting adequate sleep, to eating a healthy di...
NOV 01, 2019
Cardiology
NOV 01, 2019
Meal Timing May Have a Profound Influence on Your Workout
A new study, published in the Journal of Clinical Endocrinology and Metabolism, sought to examine the relationship between meal timing, fat storage, and in...
DEC 01, 2019
Plants & Animals
DEC 01, 2019
Blue Whales Exhibit 'Extremely Low' Heart Rates When Performing Deep Dives
Blue whales have a reputation for being massive, and as far as we know, they’re the largest living animal in existence today. Perhaps unsurprisingly,...
FEB 05, 2020
Cardiology
FEB 05, 2020
Protein-Rich Foods May Damage Heart Health
High-protein diets are becoming more and more popular as a method to both increase muscle mass and lose weight. Now however, new research is showing that e...
Loading Comments...