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
Conclusion: Macrophage polarization deserves better investigations as the therapeutic target for the
development of novel drugs against myocardial injury.