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DNA Damage Response and Autophagy: A Meaningful Partnership
Autophagy and the DNA damage response (DDR) are biological processes essential for cellular and organismal homeostasis. Herein, we summarize and discuss emerging evidence linking DDR to autophagy. We highlight published data suggesting that autophagy is activated by DNA damage and is required for se...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2016
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5116470/ https://www.ncbi.nlm.nih.gov/pubmed/27917193 http://dx.doi.org/10.3389/fgene.2016.00204 |
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author | Eliopoulos, Aristides G. Havaki, Sophia Gorgoulis, Vassilis G. |
author_facet | Eliopoulos, Aristides G. Havaki, Sophia Gorgoulis, Vassilis G. |
author_sort | Eliopoulos, Aristides G. |
collection | PubMed |
description | Autophagy and the DNA damage response (DDR) are biological processes essential for cellular and organismal homeostasis. Herein, we summarize and discuss emerging evidence linking DDR to autophagy. We highlight published data suggesting that autophagy is activated by DNA damage and is required for several functional outcomes of DDR signaling, including repair of DNA lesions, senescence, cell death, and cytokine secretion. Uncovering the mechanisms by which autophagy and DDR are intertwined provides novel insight into the pathobiology of conditions associated with accumulation of DNA damage, including cancer and aging, and novel concepts for the development of improved therapeutic strategies against these pathologies. |
format | Online Article Text |
id | pubmed-5116470 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-51164702016-12-02 DNA Damage Response and Autophagy: A Meaningful Partnership Eliopoulos, Aristides G. Havaki, Sophia Gorgoulis, Vassilis G. Front Genet Genetics Autophagy and the DNA damage response (DDR) are biological processes essential for cellular and organismal homeostasis. Herein, we summarize and discuss emerging evidence linking DDR to autophagy. We highlight published data suggesting that autophagy is activated by DNA damage and is required for several functional outcomes of DDR signaling, including repair of DNA lesions, senescence, cell death, and cytokine secretion. Uncovering the mechanisms by which autophagy and DDR are intertwined provides novel insight into the pathobiology of conditions associated with accumulation of DNA damage, including cancer and aging, and novel concepts for the development of improved therapeutic strategies against these pathologies. Frontiers Media S.A. 2016-11-21 /pmc/articles/PMC5116470/ /pubmed/27917193 http://dx.doi.org/10.3389/fgene.2016.00204 Text en Copyright © 2016 Eliopoulos, Havaki and Gorgoulis. 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) or licensor 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 Eliopoulos, Aristides G. Havaki, Sophia Gorgoulis, Vassilis G. DNA Damage Response and Autophagy: A Meaningful Partnership |
title | DNA Damage Response and Autophagy: A Meaningful Partnership |
title_full | DNA Damage Response and Autophagy: A Meaningful Partnership |
title_fullStr | DNA Damage Response and Autophagy: A Meaningful Partnership |
title_full_unstemmed | DNA Damage Response and Autophagy: A Meaningful Partnership |
title_short | DNA Damage Response and Autophagy: A Meaningful Partnership |
title_sort | dna damage response and autophagy: a meaningful partnership |
topic | Genetics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5116470/ https://www.ncbi.nlm.nih.gov/pubmed/27917193 http://dx.doi.org/10.3389/fgene.2016.00204 |
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