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The Histone Code of Senescence

Senescence is the end point of a complex cellular response that proceeds through a set of highly regulated steps. Initially, the permanent cell-cycle arrest that characterizes senescence is a pro-survival response to irreparable DNA damage. The maintenance of this prolonged condition requires the ad...

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Detalles Bibliográficos
Autores principales: Paluvai, Harikrishnareddy, Di Giorgio, Eros, Brancolini, Claudio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072776/
https://www.ncbi.nlm.nih.gov/pubmed/32085582
http://dx.doi.org/10.3390/cells9020466
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author Paluvai, Harikrishnareddy
Di Giorgio, Eros
Brancolini, Claudio
author_facet Paluvai, Harikrishnareddy
Di Giorgio, Eros
Brancolini, Claudio
author_sort Paluvai, Harikrishnareddy
collection PubMed
description Senescence is the end point of a complex cellular response that proceeds through a set of highly regulated steps. Initially, the permanent cell-cycle arrest that characterizes senescence is a pro-survival response to irreparable DNA damage. The maintenance of this prolonged condition requires the adaptation of the cells to an unfavorable, demanding and stressful microenvironment. This adaptation is orchestrated through a deep epigenetic resetting. A first wave of epigenetic changes builds a dam on irreparable DNA damage and sustains the pro-survival response and the cell-cycle arrest. Later on, a second wave of epigenetic modifications allows the genomic reorganization to sustain the transcription of pro-inflammatory genes. The balanced epigenetic dynamism of senescent cells influences physiological processes, such as differentiation, embryogenesis and aging, while its alteration leads to cancer, neurodegeneration and premature aging. Here we provide an overview of the most relevant histone modifications, which characterize senescence, aging and the activation of a prolonged DNA damage response.
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spelling pubmed-70727762020-03-19 The Histone Code of Senescence Paluvai, Harikrishnareddy Di Giorgio, Eros Brancolini, Claudio Cells Review Senescence is the end point of a complex cellular response that proceeds through a set of highly regulated steps. Initially, the permanent cell-cycle arrest that characterizes senescence is a pro-survival response to irreparable DNA damage. The maintenance of this prolonged condition requires the adaptation of the cells to an unfavorable, demanding and stressful microenvironment. This adaptation is orchestrated through a deep epigenetic resetting. A first wave of epigenetic changes builds a dam on irreparable DNA damage and sustains the pro-survival response and the cell-cycle arrest. Later on, a second wave of epigenetic modifications allows the genomic reorganization to sustain the transcription of pro-inflammatory genes. The balanced epigenetic dynamism of senescent cells influences physiological processes, such as differentiation, embryogenesis and aging, while its alteration leads to cancer, neurodegeneration and premature aging. Here we provide an overview of the most relevant histone modifications, which characterize senescence, aging and the activation of a prolonged DNA damage response. MDPI 2020-02-18 /pmc/articles/PMC7072776/ /pubmed/32085582 http://dx.doi.org/10.3390/cells9020466 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Paluvai, Harikrishnareddy
Di Giorgio, Eros
Brancolini, Claudio
The Histone Code of Senescence
title The Histone Code of Senescence
title_full The Histone Code of Senescence
title_fullStr The Histone Code of Senescence
title_full_unstemmed The Histone Code of Senescence
title_short The Histone Code of Senescence
title_sort histone code of senescence
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072776/
https://www.ncbi.nlm.nih.gov/pubmed/32085582
http://dx.doi.org/10.3390/cells9020466
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