TY - JOUR
T1 - Cell biological mechanisms in regulation of the post-infarction inflammatory response
AU - Frangogiannis, Nikolaos G.
N1 - Funding Information:
Dr Frangogiannis’ laboratory is supported by NIH Grants R01 HL76246 and R01 HL85440 , and by Department of Defense Grants PR151134 and PR151029 .
Publisher Copyright:
© 2017 Elsevier Ltd
PY - 2018/2
Y1 - 2018/2
N2 - Inflammation plays a crucial role in cardiac repair, but may also extend ischemic injury and contribute to post-infarction remodeling. This review manuscript discusses recent advances in our understanding of the cell biology of the post-infarction inflammatory response. Recently published studies demonstrated that the functional repertoire of inflammatory and reparative cells may extend beyond the roles suggested by traditional teachings. Neutrophils may play an important role in cardiac repair by driving macrophages toward a reparative phenotype. Subsets of activated fibroblasts have been implicated in protection of ischemic cardiomyocytes, in phagocytosis of apoptotic cells, and in regulation of inflammation. Dissection of the cellular effectors of cardiac repair is critical in order to develop new therapeutic strategies for patients with acute myocardial infarction.
AB - Inflammation plays a crucial role in cardiac repair, but may also extend ischemic injury and contribute to post-infarction remodeling. This review manuscript discusses recent advances in our understanding of the cell biology of the post-infarction inflammatory response. Recently published studies demonstrated that the functional repertoire of inflammatory and reparative cells may extend beyond the roles suggested by traditional teachings. Neutrophils may play an important role in cardiac repair by driving macrophages toward a reparative phenotype. Subsets of activated fibroblasts have been implicated in protection of ischemic cardiomyocytes, in phagocytosis of apoptotic cells, and in regulation of inflammation. Dissection of the cellular effectors of cardiac repair is critical in order to develop new therapeutic strategies for patients with acute myocardial infarction.
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U2 - 10.1016/j.cophys.2017.09.001
DO - 10.1016/j.cophys.2017.09.001
M3 - Review article
AN - SCOPUS:85051008632
SN - 2468-8681
VL - 1
SP - 7
EP - 13
JO - Current Opinion in Physiology
JF - Current Opinion in Physiology
ER -