Cellular senescence in ageing: from mechanisms to therapeutic opportunities
Author: Raffaella Di Micco1, Valery Krizhanovsky2, Darren Baker3,4, Fabrizio d'Adda di Fagagna5,6
Affiliation:
1 San Raffaele Telethon Institute for Gene Therapy (SR-TIGET), IRCCS San Raffaele Scientific Institute, Milan, Italy. dimicco.raffaella@hsr.it.
2 Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.
3 Department of Pediatrics, Mayo Clinic, Rochester, MN, USA.
4 Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, USA.
5 IFOM - The FIRC Institute of Molecular Oncology, Milan, Italy. fabrizio.dadda@ifom.eu.
6 Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche, Pavia, Italy. fabrizio.dadda@ifom.eu.
Conference/Journal: Nat Rev Mol Cell Biol
Date published: 2020 Dec 16
Other:
Special Notes: doi: 10.1038/s41580-020-00314-w. , Word Count: 146
Cellular senescence, first described in vitro in 1961, has become a focus for biotech companies that target it to ameliorate a variety of human conditions. Eminently characterized by a permanent proliferation arrest, cellular senescence occurs in response to endogenous and exogenous stresses, including telomere dysfunction, oncogene activation and persistent DNA damage. Cellular senescence can also be a controlled programme occurring in diverse biological processes, including embryonic development. Senescent cell extrinsic activities, broadly related to the activation of a senescence-associated secretory phenotype, amplify the impact of cell-intrinsic proliferative arrest and contribute to impaired tissue regeneration, chronic age-associated diseases and organismal ageing. This Review discusses the mechanisms and modulators of cellular senescence establishment and induction of a senescence-associated secretory phenotype, and provides an overview of cellular senescence as an emerging opportunity to intervene through senolytic and senomorphic therapies in ageing and ageing-associated diseases.
PMID: 33328614 DOI: 10.1038/s41580-020-00314-w
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