Journal
GENES & DEVELOPMENT
Volume 34, Issue 23-24, Pages 1565-1576Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.343129.120
Keywords
senescence; SASP; inflammation; cancer; aging; disease; senolytics; senomorphics; therapeutics
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Funding
- Medical Research College [MC_U120085810]
- MRC [MC_U120085810] Funding Source: UKRI
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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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