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. 2019 Dec 30;12:611. doi: 10.1186/s13071-019-3866-0

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© The Author(s) 2019

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — miRNAs regulate the HSC activation and schistosomiasis liver fibrosis through modulating TGF-β/SMAD signaling pathway. The key event of schistosomiasis liver fibrosis is the HSC activation, where the TGF-β/SMAD signaling pathway plays a vital role in the process. After schistosome infection, soluble egg antigen (SEA) induces macrophages to secret TGF-β [119, 120], which is the classic fibrogenic cytokine that promotes the activation of HSC. TGF-β binds to the receptors leading to phosphorylation of Smad-2 and Smad-3, followed by aggregation with Smad-4 and subsequently drives the expression of Smad-7 which negatively regulates TGF-β/SMAD signaling by blocking the TGF-β type I receptor (TβRΙ). Upon HSC activation, synthesis of ECM proteins is enhanced, especially collagen I and II, therefore resulting in liver fibrosis. Dysregulation of miRNAs regulate the TGF-β/SMAD signaling pathway to influence the activation of HSC and therefore exert a pro-fibrosis (miR-21, miR-96 and miR-351) or anti-fibrosis (miR-203-3p, miR-454, let-7b and miR-29b-3p) role in schistosomiasis