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.