Closer to a CURE for heart failure? Scientists find a way to create cells that beat harder, faster and stronger

November 10, 2016

After a heart attack, muscle tissue is damaged, preventing blood flow
Current methods can typically only convert 10% of scar into muscle
But a new study has identified two chemicals that do a better job
Researchers claim this could be a big step towards a heart failure cure

Mia De Graaf For Dailymail.com

Published:
18:10 EST, 10 November 2016

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Updated:
18:10 EST, 10 November 2016

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Scientists have created heart cells that can beat harder, faster and stronger than any current technology.

A team at San Francisco’s Gladstone Institute tested 5,500 different chemicals before identifying two that can turn scar tissue into healthy heart muscle.

The development could transform prospects for heart surgery patients.

By turning one type of adult cell into another in the heart, the Gladstone scientists have been able to regenerate muscle cells in mice

Heart failure afflicts 5.7 million Americans, costs the country $30.7 billion every year, and has no cures.

After a heart attack, connective tissue forms scar tissue at the site of the injury, contributing to heart failure.

When heart muscle is damaged, the body is unable to repair the dead or injured cells.

By turning one type of adult cell into another in the heart, the Gladstone scientists have been able to regenerate muscle cells in mice.

It means they could treat, and perhaps one day cure, heart failure.

Current methods are effective. Surgeons reprogram connective tissue cells into heart muscle cells using certain proteins.

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But usually only 10 percent of cells convert from scar tissue into muscle.

Senior author Dr Deepak Srivastava hopes this new study could drive up that figure.

‘While our original process for direct cardiac reprogramming with GMT has been promising, it could be more efficient,’ Dr Deepak Srivastava, director of the Gladstone Institute of Cardiovascular Disease, said.

‘With our screen, we discovered that chemically inhibiting two biological pathways active in embryonic formation improves the speed, quantity, and quality of the heart cells produced from our original process.’

In a more complicated procedure, the team also managed to improve the quality of redirecting cells to merge with the other heart cells, allowing for smoother functioning.

‘Heart failure afflicts many people worldwide, and we still do not have an effective treatment for patients suffering from this disease,’ said Dr Tamer Mohamed first author on the study and a former postdoctoral scholar at Gladstone.

‘With our enhanced method of direct cardiac reprogramming, we hope to combine gene therapy with drugs to create better treatments for patients suffering from this devastating disease.’