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]

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.