Limiting Fibrosis after Myocardial Infarction

A recent study by Kobayashi and colleagues1 showed that a secreted protein may be a therapeutic target for limiting fibrosis and improving function after myocardial infarction. Myocardial infarction is a catastrophic event, causing damage to the heart wall — usually, the wall of the left ventricular chamber, which pumps blood into the circulation to perfuse other vital organs. This can lead to heart failure and, consequently, to disability or death. The wound, caused by necrosis and apoptosis after coronary-artery occlusion, triggers the healing process, resulting in a strong fibrotic scar and the restoration of pump function.

Healing is accomplished through . . .


From the Division of Cardiology, Department of Medicine and Cardiovascular Research Group, Faculty of Medicine, University of Alberta, Edmonton, Canada
http://content.nejm.org/cgi/content/full/360/15/1567