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Epigenetic Basis of Cellular Senescence and Its Implications in Aging
Cellular senescence is a tumor suppressive response that has become recognized as a major contributor of tissue aging. Senescent cells undergo a stable proliferative arrest that protects against neoplastic transformation, but acquire a secretory phenotype that has long-term deleterious effects. Stud...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5748661/ https://www.ncbi.nlm.nih.gov/pubmed/29186801 http://dx.doi.org/10.3390/genes8120343 |
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author | Nacarelli, Timothy Liu, Pingyu Zhang, Rugang |
author_facet | Nacarelli, Timothy Liu, Pingyu Zhang, Rugang |
author_sort | Nacarelli, Timothy |
collection | PubMed |
description | Cellular senescence is a tumor suppressive response that has become recognized as a major contributor of tissue aging. Senescent cells undergo a stable proliferative arrest that protects against neoplastic transformation, but acquire a secretory phenotype that has long-term deleterious effects. Studies are still unraveling the effector mechanisms that underlie these senescence responses with the goal to identify therapeutic interventions. Such effector mechanisms have been linked to the dramatic remodeling in the epigenetic and chromatin landscape that accompany cellular senescence. We discuss these senescence-associated epigenetic changes and their impact on the senescence phenotypes, notably the proliferative arrest and senescence associated secretory phenotype (SASP). We also explore possible epigenetic targets to suppress the deleterious effects of senescent cells that contribute towards aging. |
format | Online Article Text |
id | pubmed-5748661 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-57486612018-01-07 Epigenetic Basis of Cellular Senescence and Its Implications in Aging Nacarelli, Timothy Liu, Pingyu Zhang, Rugang Genes (Basel) Review Cellular senescence is a tumor suppressive response that has become recognized as a major contributor of tissue aging. Senescent cells undergo a stable proliferative arrest that protects against neoplastic transformation, but acquire a secretory phenotype that has long-term deleterious effects. Studies are still unraveling the effector mechanisms that underlie these senescence responses with the goal to identify therapeutic interventions. Such effector mechanisms have been linked to the dramatic remodeling in the epigenetic and chromatin landscape that accompany cellular senescence. We discuss these senescence-associated epigenetic changes and their impact on the senescence phenotypes, notably the proliferative arrest and senescence associated secretory phenotype (SASP). We also explore possible epigenetic targets to suppress the deleterious effects of senescent cells that contribute towards aging. MDPI 2017-11-24 /pmc/articles/PMC5748661/ /pubmed/29186801 http://dx.doi.org/10.3390/genes8120343 Text en © 2017 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 Nacarelli, Timothy Liu, Pingyu Zhang, Rugang Epigenetic Basis of Cellular Senescence and Its Implications in Aging |
title | Epigenetic Basis of Cellular Senescence and Its Implications in Aging |
title_full | Epigenetic Basis of Cellular Senescence and Its Implications in Aging |
title_fullStr | Epigenetic Basis of Cellular Senescence and Its Implications in Aging |
title_full_unstemmed | Epigenetic Basis of Cellular Senescence and Its Implications in Aging |
title_short | Epigenetic Basis of Cellular Senescence and Its Implications in Aging |
title_sort | epigenetic basis of cellular senescence and its implications in aging |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5748661/ https://www.ncbi.nlm.nih.gov/pubmed/29186801 http://dx.doi.org/10.3390/genes8120343 |
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