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Research reveals unknown mechanism of atherosclerosis
Many people suffer from hardening of the arteries without knowing it and being aware of the possible consequences. Atherosclerosis is an extremely serious complaint, which in the worst case can result in a stroke or heart attack. In a current study, previously unknown mechanisms have been uncovered that have a direct impact on the risk of stroke and heart attack with hardening of the arteries. This also opens up new approaches to treatment.
An international research team led by Oliver Söhnlein from the Ludwig Maximilians University in Munich (LMU) has investigated the role of so-called neutrophils in atherosclerosis in the current study and found surprising results. These special cells of the innate immune system cause the deposited plaques to detach from the cell walls and can subsequently lead to a heart attack or stroke. The researchers have also already developed a peptide that stops the fatal process, according to the LMU.
Neutrophils lead to cell death
The neutrophils play an important role in the derailing immune response and the inflammation caused by hardening of the arteries, explains the study leader. "With every inflammation there is collateral damage, since the neutrophils, cells of the immune system, also damage the tissue," Söhnlein continues. For the first time, the researchers were able to demonstrate how the neutrophils cause this tissue damage and trigger cell death that has not yet been described.
Destabilization of the deposits
Deposits on the inner wall of the blood vessels are the main characteristic of arterial calcification. These trigger a reaction of the immune system, which then derails and causes inflammation. “It becomes dangerous if the deposit, also known as plaque, detaches from the wall of the vessel,” the researchers explain. This could lead to a heart attack or stroke. The neutrophils in turn make a significant contribution to the destabilization of the plaques and thus increase the risk.
Muscle cells are killed
When the neutrophils are activated in the muscle cells that sit directly under the wall of the plaque, they release their DNA and thus histones, which are highly charged and cytotoxic, reports the research team. "The histones kill the neighboring cells, in the case of atherosclerosis they are the smooth muscle cells," continues Oliver Söhnlein. The cell death is triggered by holes that drill the histones into the membrane of the muscle cells. Liquid enters the cell through the holes until it bursts. When the muscle cell dies, the deposits are no longer stabilized and detach from the vessel wall.
New active ingredient developed
However, the international research team has succeeded in using the “molecular modeling” technique to generate a peptide that binds to the histones and thus removes their toxic function, according to the LMU. This can stop the fateful process that can ultimately lead to a stroke or heart attack. The underlying mechanism of action can also be applied to other diseases with chronic inflammation, such as arthritis and chronic intestinal inflammation, emphasizes the study leader. A patent has already been filed for the peptide. (fp)
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