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Microbiome–metabolome reveals the contribution of gut–kidney axis on kidney disease
Dysbiosis represents changes in composition and structure of the gut microbiome community (microbiome), which may dictate the physiological phenotype (health or disease). Recent technological advances and efforts in metagenomic and metabolomic analyses have led to a dramatical growth in our understa...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6317198/ https://www.ncbi.nlm.nih.gov/pubmed/30602367 http://dx.doi.org/10.1186/s12967-018-1756-4 |
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author | Chen, Yuan-Yuan Chen, Dan-Qian Chen, Lin Liu, Jing-Ru Vaziri, Nosratola D. Guo, Yan Zhao, Ying-Yong |
author_facet | Chen, Yuan-Yuan Chen, Dan-Qian Chen, Lin Liu, Jing-Ru Vaziri, Nosratola D. Guo, Yan Zhao, Ying-Yong |
author_sort | Chen, Yuan-Yuan |
collection | PubMed |
description | Dysbiosis represents changes in composition and structure of the gut microbiome community (microbiome), which may dictate the physiological phenotype (health or disease). Recent technological advances and efforts in metagenomic and metabolomic analyses have led to a dramatical growth in our understanding of microbiome, but still, the mechanisms underlying gut microbiome–host interactions in healthy or diseased state remain elusive and their elucidation is in infancy. Disruption of the normal gut microbiota may lead to intestinal dysbiosis, intestinal barrier dysfunction, and bacterial translocation. Excessive uremic toxins are produced as a result of gut microbiota alteration, including indoxyl sulphate, p-cresyl sulphate, and trimethylamine-N-oxide, all implicated in the variant processes of kidney diseases development. This review focuses on the pathogenic association between gut microbiota and kidney diseases (the gut–kidney axis), covering CKD, IgA nephropathy, nephrolithiasis, hypertension, acute kidney injury, hemodialysis and peritoneal dialysis in clinic. Targeted interventions including probiotic, prebiotic and symbiotic measures are discussed for their potential of re-establishing symbiosis, and more effective strategies for the treatment of kidney diseases patients are suggested. The novel insights into the dysbiosis of the gut microbiota in kidney diseases are helpful to develop novel therapeutic strategies for preventing or attenuating kidney diseases and complications. [Image: see text] |
format | Online Article Text |
id | pubmed-6317198 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-63171982019-01-08 Microbiome–metabolome reveals the contribution of gut–kidney axis on kidney disease Chen, Yuan-Yuan Chen, Dan-Qian Chen, Lin Liu, Jing-Ru Vaziri, Nosratola D. Guo, Yan Zhao, Ying-Yong J Transl Med Review Dysbiosis represents changes in composition and structure of the gut microbiome community (microbiome), which may dictate the physiological phenotype (health or disease). Recent technological advances and efforts in metagenomic and metabolomic analyses have led to a dramatical growth in our understanding of microbiome, but still, the mechanisms underlying gut microbiome–host interactions in healthy or diseased state remain elusive and their elucidation is in infancy. Disruption of the normal gut microbiota may lead to intestinal dysbiosis, intestinal barrier dysfunction, and bacterial translocation. Excessive uremic toxins are produced as a result of gut microbiota alteration, including indoxyl sulphate, p-cresyl sulphate, and trimethylamine-N-oxide, all implicated in the variant processes of kidney diseases development. This review focuses on the pathogenic association between gut microbiota and kidney diseases (the gut–kidney axis), covering CKD, IgA nephropathy, nephrolithiasis, hypertension, acute kidney injury, hemodialysis and peritoneal dialysis in clinic. Targeted interventions including probiotic, prebiotic and symbiotic measures are discussed for their potential of re-establishing symbiosis, and more effective strategies for the treatment of kidney diseases patients are suggested. The novel insights into the dysbiosis of the gut microbiota in kidney diseases are helpful to develop novel therapeutic strategies for preventing or attenuating kidney diseases and complications. [Image: see text] BioMed Central 2019-01-03 /pmc/articles/PMC6317198/ /pubmed/30602367 http://dx.doi.org/10.1186/s12967-018-1756-4 Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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. |
spellingShingle | Review Chen, Yuan-Yuan Chen, Dan-Qian Chen, Lin Liu, Jing-Ru Vaziri, Nosratola D. Guo, Yan Zhao, Ying-Yong Microbiome–metabolome reveals the contribution of gut–kidney axis on kidney disease |
title | Microbiome–metabolome reveals the contribution of gut–kidney axis on kidney disease |
title_full | Microbiome–metabolome reveals the contribution of gut–kidney axis on kidney disease |
title_fullStr | Microbiome–metabolome reveals the contribution of gut–kidney axis on kidney disease |
title_full_unstemmed | Microbiome–metabolome reveals the contribution of gut–kidney axis on kidney disease |
title_short | Microbiome–metabolome reveals the contribution of gut–kidney axis on kidney disease |
title_sort | microbiome–metabolome reveals the contribution of gut–kidney axis on kidney disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6317198/ https://www.ncbi.nlm.nih.gov/pubmed/30602367 http://dx.doi.org/10.1186/s12967-018-1756-4 |
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