Myeloid Cells in Myocardial Ischemic Injury: The Role of the Macrophage Migration Inhibitory Factor

TL;DR

This paper reviews how macrophage migration inhibitory factor (MIF) influences myeloid cells during heart injury from ischemia and reperfusion.

Contribution

The paper highlights MIF's role in modulating myeloid cell metabolism and inflammation in myocardial injury, suggesting it as a potential therapeutic target.

Findings

MIF affects the metabolic profile and activity of myeloid cells during myocardial injury.

Myeloid cells are key players in the inflammatory response following ischemia and reperfusion.

MIF could serve as a therapeutic target to balance metabolism and reduce heart inflammation.

Abstract

Ischemic heart disease, manifesting as myocardial infarction (MI), remains the leading cause of death in the western world. Both ischemia and reperfusion (I/R) cause myocardial injury and result in cardiac inflammatory responses. This sterile inflammation in the myocardium consists of multiple phases, involving cell death, tissue remodeling, healing, and scar formation, modulated by various cytokines, including the macrophage migration inhibitory factor (MIF). Meanwhile, different immune cells participate in these phases, with myeloid cells acting as first responders. They migrate to the injured myocardium and regulate the initial phase of inflammation. The MIF modulates the acute inflammatory response by affecting the metabolic profile and activity of myeloid cells. This review summarizes the role of the MIF in regulating myeloid cell subsets in MI and I/R injury and discusses emerging evidence of metabolism-directed cellular inflammatory responses. Based on the multifaceted role of the MIF affecting myeloid cells in MI or I/R, the MIF can be a therapeutic target to achieve metabolic balance under pathology and alleviate inflammation in the heart.

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