Journal
CURRENT DRUG TARGETS
Volume 19, Issue 6, Pages 651-662Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1389450118666171031115025
Keywords
Myocardial infarction; inflammation; macrophage polarization; cardiac healing; molecular mechanism; drug discovery
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Funding
- General Research Fund (GRF) grants from the Research Grants Council of Hong Kong Government, China [775812M, 17120915, 17146216]
- University of Hong Kong, China
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Background: Myocardial infarction is characterized by the interruption of blood flow through the heart, directly causing mortality and disability worldwide. Cardiac macrophages exhibit distinct phenotypes (e.g., M1 or M2) and functions (e.g., proinflammatory or anti-inflammatory) in response to the alterations of myocardial microenvironment, and subsequently exacerbate or resolve inflammation in the infarcted hearts. Regulation of macrophage polarization was implicated in myocardial infarction for the quality and outcome of cardiac healing. Objective: The purpose of this review was to summarise the current understanding on the regulation of macrophage polarization in myocardial infarction and highlight the therapeutic potential of pharmacological regulators in the treatment of myocardial injury via modulating macrophage polarization. Results: Timely control of M2/M1 ratio by endogenous mediators and pharmacological regulators should help the resolution of inflammation, promote wound healing and prevent cardiac fibrosis after myocardial infarction. Conclusion: Macrophage polarization deserves better investigations as the therapeutic target for the development of novel drugs against myocardial injury.
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