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Identification of Common Genes and Pathways in Eight Fibrosis Diseases
Acute and chronic inflammation often leads to fibrosis, which is also the common and final pathological outcome of chronic inflammatory diseases. To explore the common genes and pathogenic pathways among different fibrotic diseases, we collected all the reported genes of the eight fibrotic diseases:...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7844395/ https://www.ncbi.nlm.nih.gov/pubmed/33519923 http://dx.doi.org/10.3389/fgene.2020.627396 |
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author | Gu, Chang Shi, Xin Dang, Xuening Chen, Jiafei Chen, Chunji Chen, Yumei Pan, Xufeng Huang, Tao |
author_facet | Gu, Chang Shi, Xin Dang, Xuening Chen, Jiafei Chen, Chunji Chen, Yumei Pan, Xufeng Huang, Tao |
author_sort | Gu, Chang |
collection | PubMed |
description | Acute and chronic inflammation often leads to fibrosis, which is also the common and final pathological outcome of chronic inflammatory diseases. To explore the common genes and pathogenic pathways among different fibrotic diseases, we collected all the reported genes of the eight fibrotic diseases: eye fibrosis, heart fibrosis, hepatic fibrosis, intestinal fibrosis, lung fibrosis, pancreas fibrosis, renal fibrosis, and skin fibrosis. We calculated the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment scores of all fibrotic disease genes. Each gene was encoded using KEGG and GO enrichment scores, which reflected how much a gene can affect this function. For each fibrotic disease, by comparing the KEGG and GO enrichment scores between reported disease genes and other genes using the Monte Carlo feature selection (MCFS) method, the key KEGG and GO features were identified. We compared the gene overlaps among eight fibrotic diseases and connective tissue growth factor (CTGF) was finally identified as the common key molecule. The key KEGG and GO features of the eight fibrotic diseases were all screened by MCFS method. Moreover, we interestingly found overlaps of pathways between renal fibrosis and skin fibrosis, such as GO:1901890-positive regulation of cell junction assembly, as well as common regulatory genes, such as CTGF, which is the key molecule regulating fibrogenesis. We hope to offer a new insight into the cellular and molecular mechanisms underlying fibrosis and therefore help leading to the development of new drugs, which specifically delay or even improve the symptoms of fibrosis. |
format | Online Article Text |
id | pubmed-7844395 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-78443952021-01-30 Identification of Common Genes and Pathways in Eight Fibrosis Diseases Gu, Chang Shi, Xin Dang, Xuening Chen, Jiafei Chen, Chunji Chen, Yumei Pan, Xufeng Huang, Tao Front Genet Genetics Acute and chronic inflammation often leads to fibrosis, which is also the common and final pathological outcome of chronic inflammatory diseases. To explore the common genes and pathogenic pathways among different fibrotic diseases, we collected all the reported genes of the eight fibrotic diseases: eye fibrosis, heart fibrosis, hepatic fibrosis, intestinal fibrosis, lung fibrosis, pancreas fibrosis, renal fibrosis, and skin fibrosis. We calculated the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment scores of all fibrotic disease genes. Each gene was encoded using KEGG and GO enrichment scores, which reflected how much a gene can affect this function. For each fibrotic disease, by comparing the KEGG and GO enrichment scores between reported disease genes and other genes using the Monte Carlo feature selection (MCFS) method, the key KEGG and GO features were identified. We compared the gene overlaps among eight fibrotic diseases and connective tissue growth factor (CTGF) was finally identified as the common key molecule. The key KEGG and GO features of the eight fibrotic diseases were all screened by MCFS method. Moreover, we interestingly found overlaps of pathways between renal fibrosis and skin fibrosis, such as GO:1901890-positive regulation of cell junction assembly, as well as common regulatory genes, such as CTGF, which is the key molecule regulating fibrogenesis. We hope to offer a new insight into the cellular and molecular mechanisms underlying fibrosis and therefore help leading to the development of new drugs, which specifically delay or even improve the symptoms of fibrosis. Frontiers Media S.A. 2021-01-15 /pmc/articles/PMC7844395/ /pubmed/33519923 http://dx.doi.org/10.3389/fgene.2020.627396 Text en Copyright © 2021 Gu, Shi, Dang, Chen, Chen, Chen, Pan and Huang. http://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 | Genetics Gu, Chang Shi, Xin Dang, Xuening Chen, Jiafei Chen, Chunji Chen, Yumei Pan, Xufeng Huang, Tao Identification of Common Genes and Pathways in Eight Fibrosis Diseases |
title | Identification of Common Genes and Pathways in Eight Fibrosis Diseases |
title_full | Identification of Common Genes and Pathways in Eight Fibrosis Diseases |
title_fullStr | Identification of Common Genes and Pathways in Eight Fibrosis Diseases |
title_full_unstemmed | Identification of Common Genes and Pathways in Eight Fibrosis Diseases |
title_short | Identification of Common Genes and Pathways in Eight Fibrosis Diseases |
title_sort | identification of common genes and pathways in eight fibrosis diseases |
topic | Genetics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7844395/ https://www.ncbi.nlm.nih.gov/pubmed/33519923 http://dx.doi.org/10.3389/fgene.2020.627396 |
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