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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| Vydané v: | Genes & development Ročník 34; číslo 23-24; s. 1565 |
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| Hlavní autori: | , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
United States
01.12.2020
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| Predmet: | |
| ISSN: | 1549-5477, 1549-5477 |
| On-line prístup: | Zistit podrobnosti o prístupe |
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| Abstract | 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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| AbstractList | 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.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. 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. |
| Author | Birch, Jodie Gil, Jesús |
| Author_xml | – sequence: 1 givenname: Jodie surname: Birch fullname: Birch, Jodie organization: Institute of Clinical Sciences, Faculty of Medicine, Imperial College London, London W12 0NN, United Kingdom – sequence: 2 givenname: Jesús surname: Gil fullname: Gil, Jesús organization: Institute of Clinical Sciences, Faculty of Medicine, Imperial College London, London W12 0NN, United Kingdom |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33262144$$D View this record in MEDLINE/PubMed |
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| Snippet | Cellular senescence is a stress response that elicits a permanent cell cycle arrest and triggers profound phenotypic changes such as the production of a... |
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| StartPage | 1565 |
| SubjectTerms | Aging - genetics Aging - pathology Cellular Senescence - genetics Disease Susceptibility - therapy Drug Development Drug Therapy Epigenesis, Genetic Gene Expression Regulation Humans Pharmaceutical Preparations - chemistry Secretory Pathway Signal Transduction |
| Title | Senescence and the SASP: many therapeutic avenues |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/33262144 https://www.proquest.com/docview/2466296908 |
| Volume | 34 |
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