This is how our heart can heal itself

This is how our heart can heal itself

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How can the regeneration of the heart be supported?

A newly discovered protein that affects cell division in the heart could, according to a recent study, possibly be used to support heart cells in regeneration.

The University of Texas research found that a special protein can reduce heart cell division. The results of the study were published in the English-language journal "Nature".

Treatment of many diseases in prospect

Slowing down cell division in the heart could help heart cells regenerate. This would offer a whole new way to treat a variety of diseases that damage the heart muscle, including heart failure caused by viruses, poisons, high blood pressure, or heart attacks, the researchers report.

Why it is so important to regenerate the heart muscle

Current pharmaceutical treatments for heart failure (including ACE inhibitors and beta blockers) focus on trying to stop heart muscle loss. However, the increased stress damages the heart muscle and leads to the death of further cells. And there are currently no treatments to rebuild the heart muscle.

Hearts of mice regenerated

When examined in mice whose hearts had suffered damage in the first days of their lives, the researchers found nine years ago that the hearts can regenerate, driven by the division of cardiomyocytes, the cells that are responsible for the contraction force of the heart are responsible.

Regeneration ability disappears after seven days

However, this ability is completely lost at the age of seven days, an abrupt turning point at which the division of these cells slows dramatically and the cells themselves enlarge. The reasons why the cell division gradually slows down and the cells no longer divide have remained unclear, the researchers report.

What role does Meis1 play in the division of heart cells?

The research group then found in 2013 that a protein called Meis1, which falls into the category of transcription factors that regulate the activity of genes, plays a key role in stopping the division of heart cells. If the associated gene was deleted in mice, the time window for cardiac cell division increased, but only temporarily. Cardiac cells that lack the associated gene also slow down their division and stop their multiplication.

Genetically modified mice were examined

As a result, the researchers asked themselves whether there are redundant mechanisms that stop heart cell division even without Meis1. They identified a transcription factor called Hoxb13. To better understand the role of Hoxb13 in heart cells, the researchers have bred genetically modified mice in which the gene encoding Hoxb13 has been removed.

Positive effects only lasted briefly

These mice behaved similarly to those in which only the Meis1 gene was removed. The time window for the rapid division of the heart cells was increased, but still ended within a few weeks. When the researchers switched off Hoxb13 in the hearts of adult mice, their cell division resumed briefly, which was sufficient to prevent worsening after an induced heart attack. However, the resurgence was not enough to promote a significant recovery.

Elimination of both genes led to success

However, when the researchers switched off both genes for Meis1 and Hoxb13, the heart cells in the mice seemed to return to an earlier stage of development, increasing in size and increasing in size. After an induced heart attack, these mice showed a rapid improvement in the amount of blood that was excreted from the heart with each beat. Her heart function had almost returned to normal, explains the research group.

Is the protein calcineurin the solution?

Since there was clear evidence that Meis1 and Hoxb13 work together to stop heart cell division in the days after birth, the researchers looked for ways to regulate these proteins. Experiments carried out suggest that a protein called calcineurin, which is responsible for regulating the activity of other proteins, could represent just such a possibility.

There are various drugs that target calcineurin

Because calcineurin plays a key role in a variety of diseases and other ailments such as rheumatoid arthritis, schizophrenia, diabetes and organ transplants, there are already several drugs on the market that target this protein.

Stop the division of heart cells by a drug

According to the researchers, it is conceivable that further drugs could be developed that target Meis1 and Hoxb13 directly. Strategies could potentially be derived to restart the division of the heart cells by a single drug or a combination of drugs. In the future, the results of the study could lead to the lives of sick people being saved, the researchers hope. (as)

Author and source information

This text corresponds to the requirements of the medical literature, medical guidelines and current studies and has been checked by medical doctors.


  • Ngoc Uyen Nhi Nguyen, Diana C. Canseco, Feng Xiao, Yuji Nakada, Shujuan Li et al .: A calcineurin – Hoxb13 axis regulates growth mode of mammalian cardiomyocytes, in Nature (published 22.0.2020), Nature

Video: A mans heart heals itself after heart attack.. (July 2022).


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