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Epigenetic Alterations in Muscular Disorders

Epigenetic mechanisms, acting via chromatin organization, fix in time and space different transcriptional programs and contribute to the quality, stability, and heritability of cell-specific transcription programs. In the last years, great advances have been made in our understanding of mechanisms b...

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Detalles Bibliográficos
Autor principal: Lanzuolo, Chiara
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3385594/
https://www.ncbi.nlm.nih.gov/pubmed/22761545
http://dx.doi.org/10.1155/2012/256892
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author Lanzuolo, Chiara
author_facet Lanzuolo, Chiara
author_sort Lanzuolo, Chiara
collection PubMed
description Epigenetic mechanisms, acting via chromatin organization, fix in time and space different transcriptional programs and contribute to the quality, stability, and heritability of cell-specific transcription programs. In the last years, great advances have been made in our understanding of mechanisms by which this occurs in normal subjects. However, only a small part of the complete picture has been revealed. Abnormal gene expression patterns are often implicated in the development of different diseases, and thus epigenetic studies from patients promise to fill an important lack of knowledge, deciphering aberrant molecular mechanisms at the basis of pathogenesis and diseases progression. The identification of epigenetic modifications that could be used as targets for therapeutic interventions could be particularly timely in the light of pharmacologically reversion of pathological perturbations, avoiding changes in DNA sequences. Here I discuss the available information on epigenetic mechanisms that, altered in neuromuscular disorders, could contribute to the progression of the disease.
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spelling pubmed-33855942012-07-03 Epigenetic Alterations in Muscular Disorders Lanzuolo, Chiara Comp Funct Genomics Review Article Epigenetic mechanisms, acting via chromatin organization, fix in time and space different transcriptional programs and contribute to the quality, stability, and heritability of cell-specific transcription programs. In the last years, great advances have been made in our understanding of mechanisms by which this occurs in normal subjects. However, only a small part of the complete picture has been revealed. Abnormal gene expression patterns are often implicated in the development of different diseases, and thus epigenetic studies from patients promise to fill an important lack of knowledge, deciphering aberrant molecular mechanisms at the basis of pathogenesis and diseases progression. The identification of epigenetic modifications that could be used as targets for therapeutic interventions could be particularly timely in the light of pharmacologically reversion of pathological perturbations, avoiding changes in DNA sequences. Here I discuss the available information on epigenetic mechanisms that, altered in neuromuscular disorders, could contribute to the progression of the disease. Hindawi Publishing Corporation 2012 2012-06-18 /pmc/articles/PMC3385594/ /pubmed/22761545 http://dx.doi.org/10.1155/2012/256892 Text en Copyright © 2012 Chiara Lanzuolo. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Lanzuolo, Chiara
Epigenetic Alterations in Muscular Disorders
title Epigenetic Alterations in Muscular Disorders
title_full Epigenetic Alterations in Muscular Disorders
title_fullStr Epigenetic Alterations in Muscular Disorders
title_full_unstemmed Epigenetic Alterations in Muscular Disorders
title_short Epigenetic Alterations in Muscular Disorders
title_sort epigenetic alterations in muscular disorders
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3385594/
https://www.ncbi.nlm.nih.gov/pubmed/22761545
http://dx.doi.org/10.1155/2012/256892
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