Mitochondrial Dysfunction Meets Senescence

Suchira Gallage; Jesús Gil

doi:10.1016/j.tibs.2016.01.005

Mitochondrial Dysfunction Meets Senescence

Trends Biochem Sci. 2016 Mar;41(3):207-209. doi: 10.1016/j.tibs.2016.01.005. Epub 2016 Feb 11.

Authors

Suchira Gallage¹, Jesús Gil²

Affiliations

¹ Cell Proliferation Group, MRC Clinical Sciences Centre, Imperial College London, Hammersmith Campus, London W12 0NN, UK.
² Cell Proliferation Group, MRC Clinical Sciences Centre, Imperial College London, Hammersmith Campus, London W12 0NN, UK. Electronic address: jesus.gil@csc.mrc.ac.uk.

PMID: 26874922
DOI: 10.1016/j.tibs.2016.01.005

Abstract

Cellular senescence and mitochondrial dysfunction are hallmarks of ageing, but until now their relationship has not been clear. Recent work by Wiley et al. shows that mitochondrial defects can cause a distinct senescence phenotype termed MiDAS (mitochondrial dysfunction-associated senescence). MiDAS has a specific secretome that is able to drive some of the aging phenotypes. These findings suggest novel therapeutic opportunities for treating age-related pathologies.

Keywords: SASP; Senescence; Sirtuins; ageing; mitochondria; secretome.

Publication types

Comment

MeSH terms

Aging*
Cellular Senescence*
Humans
Mitochondria
Phenotype

Grants and funding

MC_U120085810/MRC_/Medical Research Council/United Kingdom