2023-08-26 14:55:39
After a heart attack, severe scarring of the heart muscle can occur, which is caused by inflammatory reactions. Together with Australian colleagues, researchers at Med-Uni Graz have found a factor that controls this so-called cardiac fibrosis. If it is possible to influence it, heart attacks could heal with less scarring – which leads to reduced heart performance.
Stiffening and loss threaten
If the heart tissue does not receive enough blood during a heart attack, it quickly begins to die. Provided that the affected coronary artery is opened again quickly enough, the infarction can heal almost without consequences. However, if the blood flow remains insufficient, the dead heart cells are “disposed of” by cells of the immune system, which is accompanied by an inflammatory process. Connective tissue cells migrate to the wounded area and form scar tissue.
“A certain amount of scarring is necessary, the problem is that in some cases the scarring overshoots the target,” said Peter Rainer from Med-Uni Graz.
If there is an excessive formation of scar tissue – a so-called fibrosis – there is a risk of heart failure due to the progressive stiffening of the heart muscle and the loss of functioning muscle tissue serious consequences of cardiac fibrosis.
A matrix protein may be involved
There are currently no direct therapies to regulate this undesirable proliferation of connective tissue in the heart. A connection between inflammation and fibrosis in the heart has been known for a long time, but the detailed mechanism is still unclear. Researchers like Rainer’s team and their international colleagues want to find out how cells that migrate into the heart during an inflammatory reaction after a heart attack contribute to the development of fibrosis. They published their latest findings on what happens in the “Journal of the American College of Cardiology”.
The international research consortium led by Graz had already recognized that the extracellular matrix protein 1 (ECM1) might be involved in cardiac fibrosis, because they found that this value increased rapidly after a heart attack. As was shown in further preclinical studies by the international team, this happens at the same time as inflammatory cells migrate into the heart muscle. The researchers were able to show that these immune cells secrete ECM1. “This protein activates connective tissue cells that produce collagen and thus contributes directly to scarring,” explained Rainer.
ECM1
On closer examination, the team identified a receptor in these cells that is most likely responsible for the observed effects – the LRP1 receptor. According to Rainer, it serves as a mediator between the inflammatory and connective tissue cells and should regulate wound healing and scarring. “A therapeutic influence on ECM1 and the underlying signaling pathway could thus improve healing after a heart attack and prevent excessive scarring,” said Rainer optimistically.
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