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Emerging roles of extracellular vesicles in cellular senescence and aging

Cellular senescence is a cellular program that prevents the proliferation of cells at risk of neoplastic transformation. On the other hand, age‐related accumulation of senescent cells promotes aging at least partially due to the senescence‐associated secretory phenotype, whereby cells secrete high l...

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Detalles Bibliográficos
Autor principal: Takasugi, Masaki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5847882/
https://www.ncbi.nlm.nih.gov/pubmed/29392820
http://dx.doi.org/10.1111/acel.12734
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author Takasugi, Masaki
author_facet Takasugi, Masaki
author_sort Takasugi, Masaki
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description Cellular senescence is a cellular program that prevents the proliferation of cells at risk of neoplastic transformation. On the other hand, age‐related accumulation of senescent cells promotes aging at least partially due to the senescence‐associated secretory phenotype, whereby cells secrete high levels of inflammatory cytokines, chemokines, and matrix metalloproteinases. Emerging evidence, however, indicates that extracellular vesicles (EVs) are important mediators of the effects of senescent cells on their microenvironment. Senescent cells secrete more EphA2 and DNA via EVs, which can promote cancer cell proliferation and inflammation, respectively. Extracellular vesicles secreted from DNA‐damaged cells can also affect telomere regulation. Furthermore, it has now become clear that EVs actually play important roles in many aspects of aging. This review is intended to summarize these recent progresses, with emphasis on relationships between cellular senescence and EVs.
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spelling pubmed-58478822018-04-01 Emerging roles of extracellular vesicles in cellular senescence and aging Takasugi, Masaki Aging Cell Review Cellular senescence is a cellular program that prevents the proliferation of cells at risk of neoplastic transformation. On the other hand, age‐related accumulation of senescent cells promotes aging at least partially due to the senescence‐associated secretory phenotype, whereby cells secrete high levels of inflammatory cytokines, chemokines, and matrix metalloproteinases. Emerging evidence, however, indicates that extracellular vesicles (EVs) are important mediators of the effects of senescent cells on their microenvironment. Senescent cells secrete more EphA2 and DNA via EVs, which can promote cancer cell proliferation and inflammation, respectively. Extracellular vesicles secreted from DNA‐damaged cells can also affect telomere regulation. Furthermore, it has now become clear that EVs actually play important roles in many aspects of aging. This review is intended to summarize these recent progresses, with emphasis on relationships between cellular senescence and EVs. John Wiley and Sons Inc. 2018-02-01 2018-04 /pmc/articles/PMC5847882/ /pubmed/29392820 http://dx.doi.org/10.1111/acel.12734 Text en © 2018 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Takasugi, Masaki
Emerging roles of extracellular vesicles in cellular senescence and aging
title Emerging roles of extracellular vesicles in cellular senescence and aging
title_full Emerging roles of extracellular vesicles in cellular senescence and aging
title_fullStr Emerging roles of extracellular vesicles in cellular senescence and aging
title_full_unstemmed Emerging roles of extracellular vesicles in cellular senescence and aging
title_short Emerging roles of extracellular vesicles in cellular senescence and aging
title_sort emerging roles of extracellular vesicles in cellular senescence and aging
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5847882/
https://www.ncbi.nlm.nih.gov/pubmed/29392820
http://dx.doi.org/10.1111/acel.12734
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