Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Feb;14(1):35-52.
doi: 10.1007/s12265-020-10006-7. Epub 2020 May 15.

Chemokines in Myocardial Infarction

Bijun Chen  1 , Nikolaos G Frangogiannis  2
Affiliations
Review

Chemokines in Myocardial Infarction

Bijun Chen et al. J Cardiovasc Transl Res. 2021 Feb.

Abstract

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.

Keywords: CCL2; CXCL12; Cardiac remodeling; Chemokine; Leukocyte; Myocardial infarction.

PubMed Disclaimer

References

    1. Roth, G. A., Huffman, M. D., Moran, A. E., Feigin, V., Mensah, G. A., Naghavi, M., et al. (2015). Global and regional patterns in cardiovascular mortality from 1990 to 2013. Circulation, 132(17), 1667–1678. https://doi.org/10.1161/CIRCULATIONAHA.114.008720 . - DOI - PubMed
    1. Reimer, K. A., Lowe, J. E., Rasmussen, M. M., & Jennings, R. B. (1977). The wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs. Circulation, 56(5), 786–794. - DOI
    1. Hjalmarson, A., Elmfeldt, D., Herlitz, J., Holmberg, S., Malek, I., Nyberg, G., et al. (1981). Effect on mortality of metoprolol in acute myocardial infarction. A double-blind randomised trial. Lancet, 2(8251), 823–827. https://doi.org/10.1016/s0140-6736(81)91101-6 . - DOI - PubMed
    1. Pfeffer, M. A., Braunwald, E., Moye, L. A., Basta, L., Brown Jr., E. J., Cuddy, T. E., et al. (1992). Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators. N Engl J Med, 327(10), 669–677. - DOI
    1. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI) (1986). Lancet, 1(8478), 397-402.

Publication types

LinkOut - more resources