M2 Macrophages as a Potential Target for Antiatherosclerosis Treatment

Table 3

Receptors as potential targets for M2 polarization.

Targets	Way to affect the targets	Experiment animals or cells	Effect	Compounds or medicine	References
SR-A	+	SR-A^-/- mice	Lack of SR-A promotes M1 polarization by activating NF-κB and suppressing STAT6 signaling		[102–105]
Notch1R	-	THP-1 cells treated with Notch1R siRNA	Enhanced M2 macrophage activation and upregulated anti-inflammatory cytokine secretion	DAPT	[106]
FcγR	-	ApoE^-/-FcγRIIb^-/- mice	Upregulated Arg1 and lower iNOS expression than ApoE^-/- mice		[107, 108]
Nr1D1	+	Rev-erba knockdown mice	Macrophages obtained from Rev-erba knockdown mice present lower M2 while overexpression of Rev-erba increased the expression of M2 markers. Heme promoted M2 marker expression	Heme	[111]
Sdc-1	+	Sdc-1^+/+ and Sdc-1^−/− macrophages	Contributed to the motility that specifically induced M2 macrophage populations		[112]
KCa3.1	-	Human monocytes; ApoE^−/− mice on a C57BL/6 background	Reduced plaque rupture and luminal thrombus in carotid arteries, decrease expression of M1 markers, and enhance expression of M2 markers within atherosclerotic lesion	TRAM-34	[114]

SR-A: class A scavenger receptor; SR-A^-/- mice: SR-A-deficient mice; Notgh1R: Notch1 receptor; THP-1 cells: a human monocytic cell line; FcγR: Fcγ receptors; iNOS: inducible nitric oxide synthase; Nr1D1: Rev-erba; Sdc-1: Syndecan-1; KCa3.1: calcium-activated potassium channel; DAPT: N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester, a γ-secretase inhibitor; Sdc-1^+/+: wild-type macrophages; Sdc-1^−/− macrophages: Sdc-1-deficient macrophages.