Table 2.

Macrophages polarization in the treatment of aortic aneurysm

Agents	Experiment model	Pathway/key regulators	Treatment effect	References
Everolimus	AngII-induced AA in ApoE−/− mice	Bone marrow development of Ly6C + CCR2 + (inflammatory) monocytes	Decrease aortic dilatation	Moran et al. [25]
EDPs	CaCl2 induced AA in C57BL/6 mice	Modulating M1/M2 macrophage polarization	Promote AA	Dale et al. [28]
D-series resolvins	Elastase-induced AA in C57/B6 mice AngII-infused ApoE−/− mice	Increasing M2 macrophage polarization	Decrease in MMPs Attenuated AA formation and progression	Pope et al. [27]
Tregs	AngII-induced AA in ApoE−/− mice	Downregulated macrophage type 1–related genes and upregulated macrophage type 2–related genes	Declined proinflammatory cytokine expression and MMP-2 and MMP-9 levels and enhanced anti-inflammatory cytokine expression	Meng et al. [29]
BM-MSCs	AngII-induced AA in ApoE−/− mice	BM-MSC inhibited infiltration of M1 macrophages and preserved the construction of elastin	Decrease vascular inflammation Prevent AA expansion	Yamawaki-Ogata et al. [31]
IL-1β TNF-α	CaCl2 induced AA in C57BL/6 mice	TNF-α deletion but not IL-1β deletion, inhibited M1 macrophage polarization	Infusion of M1 polarized TNF-α−/− macrophages inhibited aortic diameter growth	Batra et al. [23]
CD31 agonist P8RI	AngII-induced AA in ApoE−/− mice	CD31 signaling promotes the switching of proinflammatory macrophages to the reparative phenotype	Promoting the resolution of intramural hematoma and the production of collagen in dissected aortas	Andreata et al. [18]
EPA and DHA	AngII-induced AA in ApoE−/− mice	Promote macrophage polarization toward the M2 phenotype	Inhibited aortic inflammation, degeneration and macrophage infiltration	Yoshihara et al. [26]

AngII angiotensin II, AA aortic aneurysm, ApoE apolipoprotein E, MMP matrix metalloproteinase, Tregs regulatory T cells, BM-MSC bone marrow derived mesenchymal stem cells, IL-1β interleukin-1β, TNF-α tumor necrosis factor-α, EPA eicosapntemacnioc acid, DHA docosahexaenoic acid