M2 Macrophages as a Potential Target for Antiatherosclerosis Treatment

Table 2

Enzymes as therapeutic targets for M2 polarization.

Targets	Way to affect the targets	Experiment animals or cells	Potential mechanism	Compounds or medicine	References
DPP	-	Mononuclear cells obtained from humans; ApoE^−/− mice	Via the SDF-1/CXCR4 signaling	Gliptins and Sitagliptin	[90, 91, 93]
HDAC9	-	LDLR^−/− and LDLR^−/−HDAC9^−/− mice	Increased accumulation of total acetylated H3 and H3K9 by the promoters of ABCA1, ABCG1, and PPARγ in macrophages		[94]
PKA	+	RAW267.4 macrophage cells			[79]
CHIT1	+	Mouse macrophage cells			[96]
GSK3α	-		Increased P-STAT6		[97]
ATGL	-	ATGL^-/- mice	Insufficient lipolysis influenced macrophage polarization to an M2 phenotype		[98]
NAMPT	-	Patients with coronary artery disease (CAD); murine bone marrow-derived macrophages	Inhibited M1 polarization in macrophages; enhance the expression of CD163 and PPAR	FK866	[99, 100]

DPP: dipeptidyl peptidase; HDAC9: histone deacetylase; PKA: protein kinase A; CHIT1: chitinase 1; GSK3α: glycogen synthase kinase; ATGL: adipose triglyceride lipase; NAMPT: nicotinamide phosphoribosyl transferase; ATGL^-/- mice: adipose triglyceride lipase-deficient mice; LDLR^−/− mice: LDL receptor-deficient mice; LDLR^−/−HDAC9^−/− mice: LDL receptor and HDAC9 double-deficient mice. +: activate or upregulate the targets; -: inhibit or downregulate the targets.