Pharmacological regulation of macrophage polarization to control the M2/M1 ratio may help resolve inflammation, promote wound healing, and prevent cardiac fibrosis after myocardial infarction.
This review highlights the therapeutic potential of targeting macrophage polarization to promote wound healing and prevent cardiac fibrosis after myocardial infarction.
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.
Cheng et al. (Wed,) conducted a review in Myocardial infarction. Pharmacological regulators of macrophage polarization was evaluated. Pharmacological regulation of macrophage polarization to control the M2/M1 ratio may help resolve inflammation, promote wound healing, and prevent cardiac fibrosis after myocardial infarction.