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...

Celý popis

Uložené v:
Podrobná bibliografia
Vydané v:Genes & development Ročník 34; číslo 23-24; s. 1565
Hlavní autori: Birch, Jodie, Gil, Jesús
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 01.12.2020
Predmet:
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
senescence
therapeutics
disease
inflammation
senolytics
cancer
aging
SASP
senomorphics
ISSN:1549-5477, 1549-5477
On-line prístup:Zistit podrobnosti o prístupe
Tagy: Pridať tag
Žiadne tagy, Buďte prvý, kto otaguje tento záznam!
Popis
Shrnutí: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.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:1549-5477
1549-5477
DOI:10.1101/gad.343129.120