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Genetic dominance of transforming growth factor-β1 polymorphisms in chronic liver disease
Chronic liver disease (CLD) is an extremely common clinical condition accompanied by sustained inflammatory response leading to tissue damage. Transforming growth factor-β1 (TGF-β1) is known as a master immune regulator in CLDs, but the association between TGF-β1 polymorphisms and CLD risk is contro...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9708878/ https://www.ncbi.nlm.nih.gov/pubmed/36466817 http://dx.doi.org/10.3389/fimmu.2022.1058532 |
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author | Cai, Xuanyan Zha, Huiyan Yang, Zhaoxu Du, Yiwen Dai, Xiaoyang Yang, Bo Wang, Jiajia He, Qiaojun Weng, Qinjie |
author_facet | Cai, Xuanyan Zha, Huiyan Yang, Zhaoxu Du, Yiwen Dai, Xiaoyang Yang, Bo Wang, Jiajia He, Qiaojun Weng, Qinjie |
author_sort | Cai, Xuanyan |
collection | PubMed |
description | Chronic liver disease (CLD) is an extremely common clinical condition accompanied by sustained inflammatory response leading to tissue damage. Transforming growth factor-β1 (TGF-β1) is known as a master immune regulator in CLDs, but the association between TGF-β1 polymorphisms and CLD risk is controversial and inconclusive, and the genetic dominance of CLDs remains unknown. In this study, the relationship between TGF-β1 polymorphisms and CLD susceptibility is systematically analyzed based on 35 eligible studies. Individuals with the TGF-β1-509 allele (TT or CT) or codon 10 allele (Pro/Pro) show an increased risk of CLDs. Subgroup analyses indicate TGF-β1-509C/T has a significant correlation with cirrhosis and chronic hepatitis C, codon 10 is associated with chronic hepatitis B occurrence, and codon 25 exhibits a relationship with autoimmune hepatitis risk. Missense mutations in G29E, A105S, D191N, and F321L of TGF-β1 are the genetic factors of HCC susceptibility. Furthermore, the TGF-β1 gene expression is significantly elevated in CLD patients, and the TGF-β1 codon 263 is located close to the region where the TGF-β1 dimerization interacts, indicating the TGF-β1 codon 263 variant may affect the secretion of TGF-β1 by altering its dimerization. Together, our findings provide new insights into the immune regulator gene TGF-β1 polymorphisms as susceptibility factors for CLD occurrence and regulators for TGF-β1 expression, which have implications for the regulation of immune factors during CLD development. |
format | Online Article Text |
id | pubmed-9708878 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-97088782022-12-01 Genetic dominance of transforming growth factor-β1 polymorphisms in chronic liver disease Cai, Xuanyan Zha, Huiyan Yang, Zhaoxu Du, Yiwen Dai, Xiaoyang Yang, Bo Wang, Jiajia He, Qiaojun Weng, Qinjie Front Immunol Immunology Chronic liver disease (CLD) is an extremely common clinical condition accompanied by sustained inflammatory response leading to tissue damage. Transforming growth factor-β1 (TGF-β1) is known as a master immune regulator in CLDs, but the association between TGF-β1 polymorphisms and CLD risk is controversial and inconclusive, and the genetic dominance of CLDs remains unknown. In this study, the relationship between TGF-β1 polymorphisms and CLD susceptibility is systematically analyzed based on 35 eligible studies. Individuals with the TGF-β1-509 allele (TT or CT) or codon 10 allele (Pro/Pro) show an increased risk of CLDs. Subgroup analyses indicate TGF-β1-509C/T has a significant correlation with cirrhosis and chronic hepatitis C, codon 10 is associated with chronic hepatitis B occurrence, and codon 25 exhibits a relationship with autoimmune hepatitis risk. Missense mutations in G29E, A105S, D191N, and F321L of TGF-β1 are the genetic factors of HCC susceptibility. Furthermore, the TGF-β1 gene expression is significantly elevated in CLD patients, and the TGF-β1 codon 263 is located close to the region where the TGF-β1 dimerization interacts, indicating the TGF-β1 codon 263 variant may affect the secretion of TGF-β1 by altering its dimerization. Together, our findings provide new insights into the immune regulator gene TGF-β1 polymorphisms as susceptibility factors for CLD occurrence and regulators for TGF-β1 expression, which have implications for the regulation of immune factors during CLD development. Frontiers Media S.A. 2022-11-16 /pmc/articles/PMC9708878/ /pubmed/36466817 http://dx.doi.org/10.3389/fimmu.2022.1058532 Text en Copyright © 2022 Cai, Zha, Yang, Du, Dai, Yang, Wang, He and Weng https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Cai, Xuanyan Zha, Huiyan Yang, Zhaoxu Du, Yiwen Dai, Xiaoyang Yang, Bo Wang, Jiajia He, Qiaojun Weng, Qinjie Genetic dominance of transforming growth factor-β1 polymorphisms in chronic liver disease |
title | Genetic dominance of transforming growth factor-β1 polymorphisms in chronic liver disease |
title_full | Genetic dominance of transforming growth factor-β1 polymorphisms in chronic liver disease |
title_fullStr | Genetic dominance of transforming growth factor-β1 polymorphisms in chronic liver disease |
title_full_unstemmed | Genetic dominance of transforming growth factor-β1 polymorphisms in chronic liver disease |
title_short | Genetic dominance of transforming growth factor-β1 polymorphisms in chronic liver disease |
title_sort | genetic dominance of transforming growth factor-β1 polymorphisms in chronic liver disease |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9708878/ https://www.ncbi.nlm.nih.gov/pubmed/36466817 http://dx.doi.org/10.3389/fimmu.2022.1058532 |
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