Review Article
M2 Macrophages as a Potential Target for Antiatherosclerosis Treatment
Table 4
Transcription factors as potential targets for M2 polarization.
| Targets | Way to affect the targets | Experiment animals or cells | Effect | Compounds or medicine | References |
| PPARγ | + | Macrophages in human carotid atherosclerotic lesions | Increased the expression of the anti-inflammatory M2 cytokine Arg1 and attenuated the iNOS/Arg1 ratio | Thiazolidinediones (TZDs) such as rosiglitazone and thiazolidinedione | [121, 122] | PPARδ | + | C57BL/6 LDLR−/− mice | Upregulated M2 cytokines, while decreasing the expression of M1 cytokines | GW1516 | [123] | NOR1 | + | Bone marrow-derived macrophages obtained from C57BL/6J mice | A direct target of STAT6 and then promoted M2 expression | | [124] | KLF4 | + | Mouse peritoneal macrophages; myeloid KLF4-deficient mice | Promoted M2 marker expression by cooperating with STAT6; related with the expression of PPARγ, thus regulating M2 polarization | Kallistatin | [70, 125] | FoxO | + | Myeloid FoxO1-/- mice | Increase IL-10 gene expression and decrease Akt phosphorylation in FoxO-deficient mice; Pdk1-FoxO1 pathway was suggested | | [130] | TLE1 | + | Human peripheral blood mononuclear cells | M2 markers including TGF-β and IL-10 were observed decreasing when TLE1 was silenced by siRNA | | [132] |
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NOR1: the neuron-derived orphan receptor 1; FoxO: forkhead transcription factors; TLE1: transducin-like enhancer of split-1; myeloid FoxO1-/- mice: generated by crossing FoxO1fl/fl mice with LysMCre mice.
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