The Shenzhen University team discovered important molecules involved in tissue repair after myocardial infarction

A research team led by Professor Liu Jie from the Medical Department of Shenzhen University recently discovered that hypoxia-induced mitotic factor (HIMF) can promote the conversion of macrophages to the M1 phenotype and aggravate myocardial infarction damage, indicating that HIMF may be a new target for the treatment of myocardial infarction

After myocardial infarction (MI) occurs, the inflammatory response promotes the removal of damaged tissues and plays an active role in the remodeling of the left ventricle

Hypoxia-induced mitosis factor (HIMF) belongs to the family of cysteine-rich resistin-like molecules (RELM) and is highly conserved in mammals

HIMF is upregulated after myocardial infarction

Researchers conducted research on the myocardial infarction model of Himf ^−/− and WT mice induced by coronary artery ligation

HIMF promotes M1 type polarization of macrophages

Through immunostaining analysis, the researchers found that HIMF is mainly produced by macrophages

In order to confirm that the improvement of Himf ^−/− heart healing results is caused by the knockout of HIMF in macrophages, they commissioned Saiye to construct a macrophage-specific HIMF knockout mouse (Himf-CKO)

Pro-inflammatory NOS2 and tissue repair-related Arg1 are considered to be functional markers of M1 and M2 macrophages, respectively

In order to study the direct effect of HIMF on macrophage transformation, the researchers also manipulated the expression of Himf in macrophages RAW264.

The mechanism of HIMF-induced M1 polarization

Since HIMF is not expressed by cardiac fibroblasts, the researchers explored the crosstalk between HIMF-overexpressing macrophages and cardiac fibroblasts

Previous studies have shown that C/EBP-homologous protein (CHOP) plays an important role in determining the polarity of macrophages

Later, they further discovered that the activation of STAT1 is related to changes in the expression of CHOP in the infarcted heart.

Given that human resistin is functionally similar to rodent HIMF, the researchers speculate that this conclusion about HIMF may be extended to resistin, so resistin is expected to become a new target for the treatment of myocardial infarction

Original Search

Li, Y.