TY - JOUR
T1 - Chemokines in Myocardial Infarction
AU - Chen, Bijun
AU - Frangogiannis, Nikolaos G.
N1 - Funding Information:
Dr Frangogiannis’ laboratory is supported by NIH R01 grants HL76246, HL85440, and HL149407, and by Department of Defense grants PR151029 and PR181464. Dr Chen is supported by an American Heart Association post-doctoral award.
Publisher Copyright:
© 2020, Springer Science+Business Media, LLC, part of Springer Nature.
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2021/2
Y1 - 2021/2
N2 - In the infarcted myocardium, cardiomyocyte necrosis triggers an intense inflammatory reaction that not only is critical for cardiac repair, but also contributes to adverse remodeling and to the pathogenesis of heart failure. Both CC and CXC chemokines are markedly induced in the infarcted heart, bind to endothelial glycosaminoglycans, and regulate leukocyte trafficking and function. ELR+ CXC chemokines (such as CXCL8) control neutrophil infiltration, whereas CC chemokines (such as CCL2) mediate recruitment of mononuclear cells. Moreover, some members of the chemokine family (such as CXCL10 and CXCL12) may mediate leukocyte-independent actions, directly modulating fibroblast and vascular cell function. This review manuscript discusses our understanding of the role of the chemokines in regulation of injury, repair, and remodeling following myocardial infarction. Although several chemokines may be promising therapeutic targets in patients with myocardial infarction, clinical implementation of chemokine-based therapeutics is hampered by the broad effects of the chemokines in both injury and repair.
AB - In the infarcted myocardium, cardiomyocyte necrosis triggers an intense inflammatory reaction that not only is critical for cardiac repair, but also contributes to adverse remodeling and to the pathogenesis of heart failure. Both CC and CXC chemokines are markedly induced in the infarcted heart, bind to endothelial glycosaminoglycans, and regulate leukocyte trafficking and function. ELR+ CXC chemokines (such as CXCL8) control neutrophil infiltration, whereas CC chemokines (such as CCL2) mediate recruitment of mononuclear cells. Moreover, some members of the chemokine family (such as CXCL10 and CXCL12) may mediate leukocyte-independent actions, directly modulating fibroblast and vascular cell function. This review manuscript discusses our understanding of the role of the chemokines in regulation of injury, repair, and remodeling following myocardial infarction. Although several chemokines may be promising therapeutic targets in patients with myocardial infarction, clinical implementation of chemokine-based therapeutics is hampered by the broad effects of the chemokines in both injury and repair.
KW - CCL2
KW - CXCL12
KW - Cardiac remodeling
KW - Chemokine
KW - Leukocyte
KW - Myocardial infarction
UR - http://www.scopus.com/inward/record.url?scp=85084707393&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85084707393&partnerID=8YFLogxK
U2 - 10.1007/s12265-020-10006-7
DO - 10.1007/s12265-020-10006-7
M3 - Review article
C2 - 32415537
AN - SCOPUS:85084707393
VL - 14
SP - 35
EP - 52
JO - Journal of Cardiovascular Translational Research
JF - Journal of Cardiovascular Translational Research
SN - 1937-5387
IS - 1
ER -