Monday , June 27 2022

How an inflammation can withstand the sick heart – healing practice


Heart failure: helps with heart failure

In the case of heart failure, also known as heart failure or heart muscle weakness, a weakening of the heart muscle leads to a reduction in the blood supply to the organs. Researchers are now reporting on how the weakened heart can be helped.

Millions of people in Germany suffer from a weak heart. As the German Society of Cardiology: Cardiac Research and Circulation eV (DGK) writes in a press release, heart failure is one of the most serious and deadly heart diseases. A research team has now shown how inflammatory cells improve the function of diseased heart muscle cells.

One of the most common causes of death in this country

Heart failure or heart failure is one of the most common causes of death in Germany and is caused by heart attacks, high blood pressure (hypertension) or heart valve defects, Hannover Medical School (MHH) said in a current press release. .

The heart can no longer pump enough blood through the body and supply organs, muscles or other tissues with enough oxygen and nutrients. Those affected often have difficulty breathing and are only able to withstand stress in a limited way in daily life.

About two million people in Germany suffer from heart failure, which is often associated with inflammation of the heart muscle tissue. This has a negative impact on the course of the disease.

Maybe inflammation also has its good side

Previous attempts to suppress inflammation with the help of medications have been unsuccessful. This provoked suspicion that inflammation could also have its good side.

A research team led by Professor Dr. Kai Wollert, head of Molecular and Translational Cardiology in the Department of Cardiology and Angiology at MHH, has demonstrated for the first time how inflammation can withstand a weak heart.

White blood cells that have migrated to the heart produce a growth factor called MYGDF, which improves the performance of heart muscle cells. The work was recently published in the renowned magazine “Circulation”.

The efficiency of heart cells decreases

Heart failure is one of the main areas of research at the Cardiology and Angiology Clinic under the direction of Professor Dr. Johann Bauersachs. “In heart failure, the weakened heart tries to compensate for its reduced pumping capacity by increasing muscle mass, that is, getting bigger,” explains Professor Wollert.

However, unlike the heart of trained athletes, this growth does not lead to better heart performance. The heart muscle cells are getting bigger, but their performance decreases and the organ becomes weaker due to permanent pressure overload. Inflammatory processes triggered by white blood cells also worsen heart function.

However, there are exceptions. In the mouse model, the researchers identified an interaction between certain inflammatory cells and heart muscle cells that protects the heart. Monocytes and macrophages play a decisive role.

“When the pressure is overloaded, these inflammatory cells release MYGDF, which inhibits the pathological growth of the heart muscle and improves the function of the heart muscle cells,” explains the cardiologist.

The calcium pump is regulated upwards

As stated in the ad, MYDGF helps weakened heart muscle cells function better again by affecting the cell’s calcium balance.

In order for the heart muscle cells to relax again after a heartbeat, calcium must be pumped back to a reservoir inside the cell. With the next heartbeat, calcium will be available again. If the heart is weak, this calcium transport is disrupted and muscle strength decreases.

“MYGDF regulates the calcium pump so that heart muscle cells can function better again,” says Dr. Mortimer Korf-Klingebiel, biologist and first author of the study.

MYGDF levels fell back to normal

The researchers examined whether all of this is also important for humans in patients with heart failure due to aortic stenosis. According to the information, the heart valve between the heart chamber and the main artery (aorta) is severely reduced in this disease, so the heart must work against the increase in pressure.

Significantly increased MYDGF levels were found in blood samples from these patients. When an artificial heart valve was inserted into the patient in the cardiac catheter laboratory, the MYGDF level sank to normal values. Therefore, pressure overload also leads to the release of MYDGF in humans.

Professor Wollert and his team emphasize that the work demonstrates the need to consider the positive aspects of inflammation when considering anti-inflammatory therapies for heart failure. In addition, growth factor MYGDF could be administered itself as a therapy for heart failure.

“It works pretty well with mice,” says the cardiologist. In any case, scientists have already applied for a patent for the use of MYGDF as a new drug for heart failure. (ads)

Information about the author and the source

This text meets the requirements of the specialized medical literature, medical guidelines, and current studies and has been reviewed by medical professionals.


  • Hannover Medical School: Help for the Weak Heart, (accessed: October 16, 2021), Hannover Medical School
  • Mortimer Korf-Klingebiel, Marc R. Reboll, Felix Polten, Natalie Weber, Felix Jäckle, Xuekun Wu, Marinos Kallikourdis, Paolo Kunderfranco, Gianluigi Condorelli, Evangelos Giannitsis, Olga S. Kustikova, Axel Schambach, Andreas Pich, Julian D. Widder, Johann Bauersachs, Joop van den Heuvel, Theresia Kraft, Yong Wang, Kai C. Wollert: Myeloid-derived growth factor protects against heart failure induced by pressure overload by preserving Sarco / Endoplasmic reticulum expression Ca2 + -ATPase in cardiomyocytes; in: Circulation, (veröffentlicht: 10.08.2021), Circulation
  • German Society of Cardiology – Cardiac and circulatory research eV: successful fight against heart failure: opportunities and challenges, (accessed: 16.10.2021), German Society of Cardiology: cardiac and circulatory research eV

Important NOTE:
This article is for guidance only and is not intended to be used for self-diagnosis or self-treatment. It cannot replace a visit to the doctor.

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