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Identification of significant modules and hub genes involved in hepatic encephalopathy using WGCNA

BACKGROUND: Hepatic encephalopathy (HE) is a reversible syndrome of brain dysfunction caused by advanced liver disease. Weighted gene co-expression network analysis (WGCNA) could establish a robust co-expression network to identify the hub genes and underlying biological functions. This study was ai...

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Autores principales: Zhang, Chihao, Luo, Guqing, Lin, Jiayun, Zhao, Zhifeng, Luo, Meng, Li, Hongjie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9685938/
https://www.ncbi.nlm.nih.gov/pubmed/36424620
http://dx.doi.org/10.1186/s40001-022-00898-3
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author Zhang, Chihao
Luo, Guqing
Lin, Jiayun
Zhao, Zhifeng
Luo, Meng
Li, Hongjie
author_facet Zhang, Chihao
Luo, Guqing
Lin, Jiayun
Zhao, Zhifeng
Luo, Meng
Li, Hongjie
author_sort Zhang, Chihao
collection PubMed
description BACKGROUND: Hepatic encephalopathy (HE) is a reversible syndrome of brain dysfunction caused by advanced liver disease. Weighted gene co-expression network analysis (WGCNA) could establish a robust co-expression network to identify the hub genes and underlying biological functions. This study was aimed to explore the potential therapeutic targets in HE by WGCNA. RESULTS: The green and brown modules were found to be significantly associated with the development of HE. Functional enrichment analyses suggested the neuroinflammation, neuroimmune, extracellular matrix (ECM), and coagulation cascade were involved in HE. CYBB and FOXO1 were calculated as hub genes, which were upregulated in the HE patients. Tamibarotene and vitamin E were suggested as possible drug candidates to alleviate HE. CONCLUSIONS: It is the first time to analyze transcriptomic data of HE by WGCNA. Our study not only promoted the current understanding of neuroinflammation in HE, but also provided the first evidence that CYBB and FOXO1 played pivotal roles in the pathogenesis of HE, which might be potential biomarkers and therapeutic targets. Tamibarotene might be a novel drug compound against HE. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s40001-022-00898-3.
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spelling pubmed-96859382022-11-25 Identification of significant modules and hub genes involved in hepatic encephalopathy using WGCNA Zhang, Chihao Luo, Guqing Lin, Jiayun Zhao, Zhifeng Luo, Meng Li, Hongjie Eur J Med Res Research BACKGROUND: Hepatic encephalopathy (HE) is a reversible syndrome of brain dysfunction caused by advanced liver disease. Weighted gene co-expression network analysis (WGCNA) could establish a robust co-expression network to identify the hub genes and underlying biological functions. This study was aimed to explore the potential therapeutic targets in HE by WGCNA. RESULTS: The green and brown modules were found to be significantly associated with the development of HE. Functional enrichment analyses suggested the neuroinflammation, neuroimmune, extracellular matrix (ECM), and coagulation cascade were involved in HE. CYBB and FOXO1 were calculated as hub genes, which were upregulated in the HE patients. Tamibarotene and vitamin E were suggested as possible drug candidates to alleviate HE. CONCLUSIONS: It is the first time to analyze transcriptomic data of HE by WGCNA. Our study not only promoted the current understanding of neuroinflammation in HE, but also provided the first evidence that CYBB and FOXO1 played pivotal roles in the pathogenesis of HE, which might be potential biomarkers and therapeutic targets. Tamibarotene might be a novel drug compound against HE. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s40001-022-00898-3. BioMed Central 2022-11-24 /pmc/articles/PMC9685938/ /pubmed/36424620 http://dx.doi.org/10.1186/s40001-022-00898-3 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/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/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://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.
spellingShingle Research
Zhang, Chihao
Luo, Guqing
Lin, Jiayun
Zhao, Zhifeng
Luo, Meng
Li, Hongjie
Identification of significant modules and hub genes involved in hepatic encephalopathy using WGCNA
title Identification of significant modules and hub genes involved in hepatic encephalopathy using WGCNA
title_full Identification of significant modules and hub genes involved in hepatic encephalopathy using WGCNA
title_fullStr Identification of significant modules and hub genes involved in hepatic encephalopathy using WGCNA
title_full_unstemmed Identification of significant modules and hub genes involved in hepatic encephalopathy using WGCNA
title_short Identification of significant modules and hub genes involved in hepatic encephalopathy using WGCNA
title_sort identification of significant modules and hub genes involved in hepatic encephalopathy using wgcna
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9685938/
https://www.ncbi.nlm.nih.gov/pubmed/36424620
http://dx.doi.org/10.1186/s40001-022-00898-3
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