Epigenetic alterations in chronic disease focusing on Behçet’s disease: Review

Abstract Objective ‘Epigenetics’ is specified as the inheritable changes in gene expression with no alterations in DNA sequences. Epigenetics is a rapidly overspreading scientific field, and the study of epigenetic regulation in chronic disease is emerging. This study aims to evaluate epigenetic cha...

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Bibliographic Details
Published in:Biomedicine & pharmacotherapy Vol. 91; pp. 526 - 533
Main Authors: Alipour, Shahriar, Nouri, Mohammad, Sakhinia, Ebrahim, Samadi, Nasser, Roshanravan, Neda, Ghavami, Abed, Khabbazi, Alireza
Format: Journal Article
Language:English
Published: France Elsevier Masson SAS 01-07-2017
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Summary:Abstract Objective ‘Epigenetics’ is specified as the inheritable changes in gene expression with no alterations in DNA sequences. Epigenetics is a rapidly overspreading scientific field, and the study of epigenetic regulation in chronic disease is emerging. This study aims to evaluate epigenetic changes including DNA methylation, histone modification, and non-coding RNAs (ncRNAs) in inflammatory disease, with focus on Behçet’s disease. In this review, first we describe the history and classification of epigenetic changes, and then the role of epigenetic alterations in chronic diseases is explained. Methods Systematic search of MEDLINE, Embase, and Cochrane Library was conducted for all comparative studies since 2000 to 2015 with the limitations of the English language. Results For a notable period of time, researchers have mainly focused on the epigenetic pathways that are involved in the modulation of inflammatory and anti-inflammatory genes. Recent studies have proposed a central role for chronic inflammation in the pathogenesis of chronic disease, including Behçet’s disease. Conclusion Studies have been reported on the epigenetic of BD showed the role of alterations in the methylation level of IRS elements; histone modifications such as H3K4me27 and H3K4me3; up regulation of miR-182 and miR-3591-3p; down regulation of miR-155, miR-638 and miR-4488 in the pathogenesis of the disease.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
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ObjectType-Review-1
ISSN:0753-3322
1950-6007
DOI:10.1016/j.biopha.2017.04.106