Figure 6 | Scientific Reports

Figure 6

From: Mir-21 Mediates the Inhibitory Effect of Ang (1–7) on AngII-induced NLRP3 Inflammasome Activation by Targeting Spry1 in lung fibroblasts

Figure 6

Schematic working hypothesis. It has been demonstrated local RAAS is activated in lung tissue of fibrosis. AngII binds with AT1R in lung fibroblasts to enhance the expression level of mir-21, the recognized pro-fibrotic factor. Mir-21 promotes ERK phosphorylation and NF-κB nuclei translocation by targeting Spry1 degradation, following NLRP3 inflammasome activation. The released proinflammatory factors (Caspase-1/IL-1) by the inflammasome pathway lead to a-colllagen I synthesis and apoptosis resisitance. ACE2 degrades AngII to produce Ang(1–7), which reverses the AngII’s profibrotic effect via downregulating mir-21. As a result, mir-21 and NLRP3 inflammasome play a key in local RAAS imbalance induced lung fibrosis.

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