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Senescence and the SASP: many therapeutic avenues

Cellular senescence is a stress response that elicits a permanent cell cycle arrest and triggers profound phenotypic changes such as the production of a bioactive secretome, referred to as the senescence-associated secretory phenotype (SASP). Acute senescence induction protects against cancer and li...

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Detalles Bibliográficos
Autores principales: Birch, Jodie, Gil, Jesús
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cold Spring Harbor Laboratory Press 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7706700/
https://www.ncbi.nlm.nih.gov/pubmed/33262144
http://dx.doi.org/10.1101/gad.343129.120
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author Birch, Jodie
Gil, Jesús
author_facet Birch, Jodie
Gil, Jesús
author_sort Birch, Jodie
collection PubMed
description Cellular senescence is a stress response that elicits a permanent cell cycle arrest and triggers profound phenotypic changes such as the production of a bioactive secretome, referred to as the senescence-associated secretory phenotype (SASP). Acute senescence induction protects against cancer and limits fibrosis, but lingering senescent cells drive age-related disorders. Thus, targeting senescent cells to delay aging and limit dysfunction, known as “senotherapy,” is gaining momentum. While drugs that selectively kill senescent cells, termed “senolytics” are a major focus, SASP-centered approaches are emerging as alternatives to target senescence-associated diseases. Here, we summarize the regulation and functions of the SASP and highlight the therapeutic potential of SASP modulation as complimentary or an alternative to current senolytic approaches.
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spelling pubmed-77067002021-06-01 Senescence and the SASP: many therapeutic avenues Birch, Jodie Gil, Jesús Genes Dev Review Cellular senescence is a stress response that elicits a permanent cell cycle arrest and triggers profound phenotypic changes such as the production of a bioactive secretome, referred to as the senescence-associated secretory phenotype (SASP). Acute senescence induction protects against cancer and limits fibrosis, but lingering senescent cells drive age-related disorders. Thus, targeting senescent cells to delay aging and limit dysfunction, known as “senotherapy,” is gaining momentum. While drugs that selectively kill senescent cells, termed “senolytics” are a major focus, SASP-centered approaches are emerging as alternatives to target senescence-associated diseases. Here, we summarize the regulation and functions of the SASP and highlight the therapeutic potential of SASP modulation as complimentary or an alternative to current senolytic approaches. Cold Spring Harbor Laboratory Press 2020-12-01 /pmc/articles/PMC7706700/ /pubmed/33262144 http://dx.doi.org/10.1101/gad.343129.120 Text en © 2020 Birch and Gil; Published by Cold Spring Harbor Laboratory Press http://creativecommons.org/licenses/by-nc/4.0/ This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.
spellingShingle Review
Birch, Jodie
Gil, Jesús
Senescence and the SASP: many therapeutic avenues
title Senescence and the SASP: many therapeutic avenues
title_full Senescence and the SASP: many therapeutic avenues
title_fullStr Senescence and the SASP: many therapeutic avenues
title_full_unstemmed Senescence and the SASP: many therapeutic avenues
title_short Senescence and the SASP: many therapeutic avenues
title_sort senescence and the sasp: many therapeutic avenues
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7706700/
https://www.ncbi.nlm.nih.gov/pubmed/33262144
http://dx.doi.org/10.1101/gad.343129.120
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