After a heart attack, the healing process can lead to increased storage of connective tissue and thus to excessive scarring of the damaged heart muscle. This so-called fibrosis in turn leads to the heart muscle gradually becoming stiff and unable to work properly, which ultimately results in heart failure. Researchers at Med Uni Graz, together with international colleagues, have now found a way to prevent the excessive formation of connective tissue after a heart attack and thus contribute to an optimal healing process.
Heart failure: fibrosis stiffens the heart muscle
If an interventional reopening of the blocked coronary arteries is performed immediately or shortly after the heart attack, it can heal almost without consequences. If the heart tissue begins to die due to the insufficient blood supply, this leads to inflammatory processes in the body. The already dead tissue cells are "disposed of" by the immune system, connective tissue cells migrate and form scar tissue at these sites. If this leads to an excessive formation of scar tissue - known as fibrosis - the resultant progressive stiffening of the heart muscle and the loss of functioning muscle tissue can lead to heart failure. Heart failure, in turn, is a disease with a high degree of suffering and a poor prognosis," describes cardiologist Peter Rainer.
This is where a recent publication in the prestigious ,,Journal of the American College of Cardiology" by an international research collaboration comes in, which may now have found one of the missing links between inflammation and scarring.
Optimal healing after myocardial infarction as a research goal
The researchers were able to show that immune cells that migrate into the heart tissue acutely after a heart attack secrete a protein (Extracellular Matrix Protein 1 - ECM1 for short). This protein activates connective tissue cells that produce collagen and thus contributes directly to scarring," explains Peter Rainer. The scientists subsequently identified a receptor on these cells that is most likely responsible for the observed effects (LRP1 receptor). In ischemic heart disease, the expression of ECM1 was significantly increased in patients’ hearts. ECM1 thus establishes a mediator between inflammatory and connective tissue cells that regulates wound healing and scarring. Therapeutic manipulation of ECM1 and the underlying signaling pathway could thus improve healing after infarction and prevent excessive scarring," says Peter Rainer, looking to the future.