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Table 2 Macrophages polarization in the treatment of aortic aneurysm

From: Diverse roles of macrophage polarization in aortic aneurysm: destruction and repair

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]
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]
  1. 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