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Immune system implicated in artery calcification – healing practice

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Atherosclerosis is a chronic inflammatory disease

atherosclerosisso a calcification of the arteriesis one of the most common causes of cardiovascular illnesses, heart attacks and strokes. A German research team has now been able to show for the first time how this can be done immune system involved in the development of hardening of the arteries and thus opens a new perspective on this widespread disease.

researchers of Ludwig-Maximilians-University of Munich have in a recent study protein identified only at the Regulation of immune cells is involved and development of atherosclerosis can brake. The results, recently published in the famous journal “Naturewere presented, open up new avenues of treatment for one of the most widespread diseases.

In atherosclerosis, chronic inflammatory processes take place

When fats such as cholesterol esters deposit on the inner wall layer of arterial blood vessels and thus restrict blood flow, doctors speak of atherosclerosis or arteriosclerosis.

This widespread disease can blood flow so severe that the oxygen supply to certain organs is impaired. Whereas previously the plates considered the only risk of the disease, recent work has revealed that in atherosclerosis chronic inflammatory processes expire.

Antibodies can protect or harm

Above all B cells of the immune system seem to play an important role in this process. You belong to the white blood cells and are part of the adaptive immune response. Above antibody immune cells can have both a protective and a detrimental effect on the body.

Protein controls atherosclerotic immune response

The working group around professor doctor Sabine Steffens from the Institute for the Prophylaxis and Epidemiology of Cardiovascular Diseases (IPEK) was able to identify a protein significantly involved in the control of the acquired immune response in atherosclerosis.

According to the scientists involved, the newly discovered protein could be suitable as a target structure for innovative therapies.

course of the study

As part of the study, the mice were given a diet that promotes the development of atherosclerosis. During the formation of the plaques, the researchers were able to document that the disease started at a very early stage. receiver called GPR55 is regulated upwards.

Mice unable to produce GPR55 stored larger amounts of plaque in the arteries.

What does the GPR55 receiver do?

According to the research team, the GPR55 receptor sends chemical signals from the outside to the inside of cells. Without this signal, B cells glow too active becoming, by which inflammatory processes are promoted.

Results verified on human plates

In addition, when examining human atherosclerotic plaques, it turned out that there were fewer GPR55 receptors in unstable deposits than in deposits that do not break off so easily from the inner wall of blood vessels. Unstable plates are considered particularly dangerousgiven one of them high risk of stroke falls short of

New insights into the disease process

“We wanted to better understand how B cells influence atherosclerotic diseases in order to prospectively develop new B cell-targeted therapies for this life-threatening disease”Explain Steffens.

“Our results suggest a protective role for the B-cell GPR55 signaling pathway in atherosclerosis, potentially also relevant to human pathophysiology”, concludes the professor. (vb)

Author and source information

This text corresponds to the specifications of the specialized medical literature, medical guidelines and current studies and has been verified by health professionals.

Author:

Graduate editor (FH) Volker Blasek

Sources:

  • Guillamat-Prats, R., Hering, D., Derle, A. et al. GPR55 in B cells limits the development of atherosclerosis and regulates plasma cell maturation. Nat Cardiovascular Res 1, 1056-1071 (2022). https://doi.org/10.1038/s44161-022-00155-0, nature.com
  • Ludwig-Maximilians-Universität Munich: Atherosclerosis: how the body regulates B cell activity (published: 11/24/2022), idw-online.de

Important note:
This article contains general advice only and should not be used for self-diagnosis or treatment. It cannot substitute a visit to the doctor.

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