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. 2022 Jan 11;7(1):e147819. doi: 10.1172/jci.insight.147819

Figure 9. Schematic representation of Ang-(1-7) mechanisms in macrophage migration and function favoring resolution of inflammation.

Figure 9

(1) Ang-(1-7) impairs the migration of neutrophils in a MasR-dependent way. (2) On the other hand, Ang-(1-7) signals through its MasR, culminating in the phosphorylation of ERK1/2 and production of CCL2, probably by resident cells. CCL2 binds to CCR2 receptor and promotes nonphlogistic monocyte migration, which can be abrogated by the blockage of CCR2 (RS504393), antagonism or absence of MasR (A779 and Mas knockout) or inhibition of ERK signaling (U0126). In addition, Ang-(1-7)/MasR takes part in the spontaneous resolution of acute inflammation induced by LPS or E. coli by promoting nonphlogistic migration of regulatory monocytes/macrophages and engaging in the removal of apoptotic neutrophils through efferocytosis (3) and bacteria through phagocytosis (4) and production of IL-10 and TGF-β. The proresolving effects summarized herein account for the endogenous role of Ang-(1-7) in the physiological resolution of inflammation. Note: red lines represent inhibitory effects. Created with BioRender.