Journal
NATURE
Volume 529, Issue 7584, Pages 37-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature16187
Keywords
-
Categories
Funding
- MINECO, Spain [SAF2012-38547, SAF2015-67369-R, PLE2009-0124, SAF2009-08374]
- Maria de Maeztu Programme for Units of Excellence in RD [MDM-2014-0370]
- AFM
- E-Rare/ERANET
- Fundacio Marato TV3
- MDA
- EU-FP7 (Myoage)
- EU-FP7 (Optistem)
- EU-FP7 (Endostem)
- DuchennePP-NL
- ISCIII, Spain [FIS-PS09/01267, FIS-PI13/02512, CP09/00184, PI14/01529]
- CIBERNED
- European Union ERC [282310-MyoPHAGY]
- Foundation Leducq
- Programa de Formacion de Personal Investigador (Spain)
- ICREA Funding Source: Custom
Ask authors/readers for more resources
During ageing, muscle stem-cell regenerative function declines. At advanced geriatric age, this decline is maximal owing to transition from a normal quiescence into an irreversible senescence state. How satellite cells maintain quiescence and avoid senescence until advanced age remains unknown. Here we report that basal autophagy is essential to maintain the stem-cell quiescent state in mice. Failure of autophagy in physiologically aged satellite cells or genetic impairment of autophagy in young cells causes entry into senescence by loss of proteostasis, increased mitochondrial dysfunction and oxidative stress, resulting in a decline in the function and number of satellite cells. Re-establishment of autophagy reverses senescence and restores regenerative functions in geriatric satellite cells. As autophagy also declines in human geriatric satellite cells, our findings reveal autophagy to be a decisive stem-cell-fate regulator, with implications for fostering muscle regeneration in sarcopenia.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available