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. 2022 May 26;44(1):881–892. doi: 10.1080/0886022X.2022.2079528

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© 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — Anti-fibrotic effects of VEGF in chronic kidney disease. VEGF can inhibit the expression of Smad3 and miR192, thereby suppressing TGF-β-induced EMT and improving renal fibrosis. VEGF stimulates NO production by PI3K/AKT and ERK pathways. NO activates sGC to synthesize cGMP, which subsequently activates PKG. PKG inhibits RhoA/ROCK pathway, thus reducing fibrosis. VEGF induces a phenotypic shift of macrophages from M0 to M2, ameliorates fibrosis and vascular rarefaction. Inhibition of VEGFR-2 can block PMT, leading to improve microvascular rarefaction and fibrosis. VEGF can also suppress the expression of inflammatory mediators. (Abbreviations: VEGF: vascular endothelial growth factor; TGF-β: transforming growth factor-β; EMT: epithelial-to-mesenchymal transition; NO: nitric oxide; sGC: soluble guanylate cyclase; PKG: cGMP dependent protein kinases; VEGFR: vascular endothelial growth factor receptor; PMT: pericyte-myofibroblast transition; PDGF: platelet-derived growth factor).