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The mTOR/p70S6K1 signaling pathway in renal fibrosis of children with immunoglobulin A nephropathy

AIM: The purpose of this study was to explore whether mTOR/p70S6K1 signaling is activated in renal fibrosis of immunoglobulin A nephropathy. METHODS: Seventy-two children with immunoglobulin A nephropathy were divided into three groups according to their clinical features and pathological grades. Si...

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Autores principales: Xu, Yuanyuan, Ling, Yihong, Yang, Fan, Deng, Jiong, Rong, Liping, Jiang, Mengjie, Jiang, Xiaoyun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5843880/
https://www.ncbi.nlm.nih.gov/pubmed/28685619
http://dx.doi.org/10.1177/1470320317717831
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author Xu, Yuanyuan
Ling, Yihong
Yang, Fan
Deng, Jiong
Rong, Liping
Jiang, Mengjie
Jiang, Xiaoyun
author_facet Xu, Yuanyuan
Ling, Yihong
Yang, Fan
Deng, Jiong
Rong, Liping
Jiang, Mengjie
Jiang, Xiaoyun
author_sort Xu, Yuanyuan
collection PubMed
description AIM: The purpose of this study was to explore whether mTOR/p70S6K1 signaling is activated in renal fibrosis of immunoglobulin A nephropathy. METHODS: Seventy-two children with immunoglobulin A nephropathy were divided into three groups according to their clinical features and pathological grades. Six normal renal specimens were included in the control group. The expression levels of angiotensin II, mTOR, p70S6K1, E-cadherin, and α-smooth muscle actin in renal tissues were determined by immunohistochemistry method, the potential correlations of these indexes and relationship between these indexes and the clinicopathological indexes were analyzed. RESULTS: Compared to the control group, the expression levels of angiotensin II, mTOR, p70S6K1, and α-smooth muscle actin were significantly higher and the expression levels of E-cadherin were lower both in glomeruli and tubulointerstitium of immunoglobulin A nephropathy children. And the most significant differences were found in the nephrotic syndrome group and pathological grade IV group. In immunoglobulin A nephropathy renal tissues, the expression levels of angiotensin II in glomeruli and tubulointerstitium were both positively correlated with the expression levels of mTOR and α- smooth muscle actin, and negatively correlated with the expression levels of E-cadherin. CONCLUSION: The mTOR/p70S6K1 signaling was activated in renal tissues of children with immunoglobulin A nephropathy, and future studies will need to address the mechanism of mTOR/p70S6K1 signaling in the progress of renal fibrosis in immunoglobulin A nephropathy.
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spelling pubmed-58438802018-03-20 The mTOR/p70S6K1 signaling pathway in renal fibrosis of children with immunoglobulin A nephropathy Xu, Yuanyuan Ling, Yihong Yang, Fan Deng, Jiong Rong, Liping Jiang, Mengjie Jiang, Xiaoyun J Renin Angiotensin Aldosterone Syst Original Article AIM: The purpose of this study was to explore whether mTOR/p70S6K1 signaling is activated in renal fibrosis of immunoglobulin A nephropathy. METHODS: Seventy-two children with immunoglobulin A nephropathy were divided into three groups according to their clinical features and pathological grades. Six normal renal specimens were included in the control group. The expression levels of angiotensin II, mTOR, p70S6K1, E-cadherin, and α-smooth muscle actin in renal tissues were determined by immunohistochemistry method, the potential correlations of these indexes and relationship between these indexes and the clinicopathological indexes were analyzed. RESULTS: Compared to the control group, the expression levels of angiotensin II, mTOR, p70S6K1, and α-smooth muscle actin were significantly higher and the expression levels of E-cadherin were lower both in glomeruli and tubulointerstitium of immunoglobulin A nephropathy children. And the most significant differences were found in the nephrotic syndrome group and pathological grade IV group. In immunoglobulin A nephropathy renal tissues, the expression levels of angiotensin II in glomeruli and tubulointerstitium were both positively correlated with the expression levels of mTOR and α- smooth muscle actin, and negatively correlated with the expression levels of E-cadherin. CONCLUSION: The mTOR/p70S6K1 signaling was activated in renal tissues of children with immunoglobulin A nephropathy, and future studies will need to address the mechanism of mTOR/p70S6K1 signaling in the progress of renal fibrosis in immunoglobulin A nephropathy. SAGE Publications 2017-07-07 /pmc/articles/PMC5843880/ /pubmed/28685619 http://dx.doi.org/10.1177/1470320317717831 Text en © The Author(s) 2017 http://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page(https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Original Article
Xu, Yuanyuan
Ling, Yihong
Yang, Fan
Deng, Jiong
Rong, Liping
Jiang, Mengjie
Jiang, Xiaoyun
The mTOR/p70S6K1 signaling pathway in renal fibrosis of children with immunoglobulin A nephropathy
title The mTOR/p70S6K1 signaling pathway in renal fibrosis of children with immunoglobulin A nephropathy
title_full The mTOR/p70S6K1 signaling pathway in renal fibrosis of children with immunoglobulin A nephropathy
title_fullStr The mTOR/p70S6K1 signaling pathway in renal fibrosis of children with immunoglobulin A nephropathy
title_full_unstemmed The mTOR/p70S6K1 signaling pathway in renal fibrosis of children with immunoglobulin A nephropathy
title_short The mTOR/p70S6K1 signaling pathway in renal fibrosis of children with immunoglobulin A nephropathy
title_sort mtor/p70s6k1 signaling pathway in renal fibrosis of children with immunoglobulin a nephropathy
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5843880/
https://www.ncbi.nlm.nih.gov/pubmed/28685619
http://dx.doi.org/10.1177/1470320317717831
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