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Breakthrough: activated cell division prevents heart failure


New Findings to Prevent Heart Failure

Heart failure (heart failure) is one of the most common fatal diseases. Researchers have now gained new insights into the prevention of the disease. They hope this will soon provide an effective procedure for treating heart failure.

One of the most common fatal diseases

Heart failure (heart failure) affects more than 20 million people worldwide and is one of the most common diseases with fatalities. In recent years, new approaches to treating heart failure have been reported. For example, scientists at the Hannover Medical School (MHH) found that more iron could help some patients because it makes the heart more resilient. Researchers from Göttingen have now gained new insights into the prevention of heart muscle weakness due to hypertension and heart valve diseases. They hope this will soon provide an effective method for treating hypertrophy-related heart failure.

Cardiac muscle cells die

Hypertrophy, the thickening of the heart muscle due to cell enlargement, is known to athletes as the “athlete's heart”, according to a statement by the University Medical Center Göttingen (UMG).

It describes a natural and reversible reaction of the heart to the permanent and intensified training stimulus.

A distinction must be made between pathological thickening of the heart wall as a result of persistent pressure, which is triggered, for example, by high blood pressure or a heart valve disease, aortic stenosis.

This is a serious condition that can lead to deterioration in heart function, heart failure and heart failure.

Heart failure is caused, among other things, by the death of cardiac muscle cells (cardiomyocytes).

Since the cardiac muscle cells can no longer divide in adulthood and therefore no replacement of the dead cardiac muscle cells is possible, the loss leads to a declining heart function and the formation of scar tissue.

Significantly longer survival rate

Researchers at the University Medical Center Göttingen (UMG) and the Indiana University School of Medicine, USA, have now managed to reactivate cell division in adult cardiac muscle cells in a mouse model.

This ability prevented heart failure when the heart was under pressure and significantly increased the survival rate.

The load is compensated for by a thickening of the heart wall, which is caused by the increase in the number of myocardial cells instead of the increase in the volume of the individual cardiac muscle cells and prevents scarring.

“Interestingly enough, by increasing the number of cells, even existing scar tissue could be reduced. This is an exciting approach to existing heart failure, ”said Priv-Doz. Dr. Karl Toischer, senior physician at the UMG Cardiology and Pneumology Clinic and first author of the study.

In the work of the Göttingen scientists, molecular mechanisms that are necessary for the division ability of the heart muscle cell were analyzed and identified in detail.

The study provides new knowledge to prevent the development of heart failure in hypertension and heart valve diseases. The results were published in the Journal of Clinical Investigation.

"We are now working on animal-based therapy methods that enable the heart muscle cell to divide," said Prof. Gerd Hasenfuß, the author of the study, director of the UMG Cardiology and Pneumology Clinic and chairman of the Göttingen Heart Center.

"Since the increased ability of the cells to divide generally entails an increased risk of developing tumors, it is important to ensure that the ability of the heart muscle cells to divide is controllable."

Hope for new procedure for the treatment of heart failure

In previous work, American researchers were able to show that the targeted formation of the protein cyclin D2 is sufficient to activate the production of heart cell DNA in genetically modified mice after a heart attack.

The resulting cell division activity of the heart cells was sufficient to improve the constitution and function of the heart in adult mice after a heart attack.

However, it remained unclear whether this therapeutic approach is also possible for other types of heart failure. Heart valve diseases either result in a pressure load when the heart has to work against the narrowed valve (aortic stenosis), or a volume load if too much blood flows back to the heart in the case of a leaky valve (aortic insufficiency).

In a previous Göttingen study, it could be shown that the mouse models were better able to compensate for an increased blood volume in the heart than an increased pressure load.

The now published study was carried out to determine whether the activation of cardiac cell division by the protein cyclin D2 in mouse models achieved similar results under increased volume and pressure loads.

The data show that the level of cardiomyocyte cell division activity in the mouse model increases with increased pressure, which in turn leads to an increased number of cardiomyocytes and an increased wall thickness despite weakened cell enlargement.

This in turn prevents heart failure and improves the survival of the mice. In contrast, the level of cardiac cell renewal neither increased, nor did the prognosis of the test mice improve with an increased volume load.

“The results of this study give hope that in the foreseeable future we will have a new, effective procedure for the treatment of heart failure caused by hypertrophy. We are pursuing this project with high pressure and want to bring it to clinical use as soon as possible, ”said Prof. Gerd Hasenfuß. (ad)

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Video: Genetic Breakthrough Identifies Heart Failure Risk in African and Latino Americans (December 2021).