TY - JOUR
T1 - Mediators Secreted by Myeloid Cells May Protect and Repair the Infarcted Myocardium
AU - Shinde, Arti V.
AU - Frangogiannis, Nikolaos G.
N1 - Publisher Copyright:
© 2015 American Heart Association, Inc.
PY - 2015/6/19
Y1 - 2015/6/19
N2 - 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.
AB - 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.
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U2 - 10.1161/CIRCRESAHA.115.306283
DO - 10.1161/CIRCRESAHA.115.306283
M3 - Review article
C2 - 26089362
AN - SCOPUS:84942934367
SN - 0009-7330
VL - 117
SP - 10
EP - 12
JO - Circulation Research
JF - Circulation Research
IS - 1
ER -