In the infarcted myocardium, cardiomyocyte necrosis activates inflammatory cascades resulting in recruitment of myeloid cells that have been suggested to extend ischemic injury, but also clear the infarct from dead cells and matrix debris, and stimulate the reparative process. A growing body of evidence suggests that subsets of myeloid cells may exert protective actions on the infarcted myocardium. A recently published study in Nature Medicine, identified myeloid-derived growth factor as an antiapoptotic and angiogenic mediator that is secreted by a subset of macrophages and may protect the infarcted heart from adverse remodeling.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine