Macrophage Polarization as a Therapeutic Target in Myocardial Infarction

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.

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.

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.

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