Myocardial infarction (MI) results in the localized death of the muscle cells that are essential for the heart’s pumping function. Depending on the extent of the damage, MI may initiate a progressive deterioration of cardiac function that ultimately leads to heart failure. Following an acute infarction, cells of the immune system induce an inflammatory reaction in the heart muscle, which promotes clearance of the damaged tissue. “Many novel post-infarct therapies are designed to inhibit the inflammation,” says Professor Oliver Söhnlein of the Institute for Cardiovascular Prevention at LMU. “However, inflammatory reactions everywhere in the body are normally self-limiting. So we set out to develop a therapeutic approach which makes use of the endogenous processes that enable the inflammation to be turned off,” he explains. A new study, which appears in the Journal of the American College of Cardiology, reports how much progress Söhnlein and his team have made so far.
Promoting self-healing after heart attack
IPEK researchers from the Söhnlein Lab have shown that a protein which stimulates the resolution of inflammatory reactions enhances cardiac repair following heart attack in both mice and pigs.
