Home
Deutsch
Advanced Search
Browse by ...
Publication overview
Contact persons
Help
Publ. Version/Full Text
DOI
PMC
 |
Open Access Gold |
|
as soon as is submitted to ZB.
REST/NRSF deficiency impairs autophagy and leads to cellular senescence in neurons.
Aging Cell, DOI: 10.1111/acel.13471:e13471 (2021)
During aging, brain performances decline. Cellular senescence is one of the aging drivers and a key feature of a variety of human age-related disorders. The transcriptional repressor RE1-silencing transcription factor (REST) has been associated with aging and higher risk of neurodegenerative disorders. However, how REST contributes to the senescence program and functional impairment remains largely unknown. Here, we report that REST is essential to prevent the senescence phenotype in primary mouse neurons. REST deficiency causes failure of autophagy and loss of proteostasis, increased oxidative stress, and higher rate of cell death. Re-establishment of autophagy reverses the main hallmarks of senescence. Our data indicate that REST has a protective role in physiological aging by regulating the autophagic flux and the senescence program in neurons, with implications for neurological disorders associated with aging.
Altmetric
Additional Metrics?
Edit extra informations
Login
Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Autophagy ; Mitochondria ; Neurons ; Oxidative Stress ; Rapamycin ; Rest/nrsf ; Senescence ; Trehalose; Rest; Abnormalities; Activation; Features
ISSN (print) / ISBN
1474-9718
e-ISSN
1474-9726
Journal
Aging Cell
Quellenangaben
Article Number: e13471
Publisher
Wiley
Publishing Place
111 River St, Hoboken 07030-5774, Nj Usa
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Developmental Genetics (IDG)
Grants
Compagnia di San Paolo Torino
Ministero Istruzione, Universita e Ricerca
Ministero della Salute Ricerca Finalizzata
Ministero Istruzione, Universita e Ricerca
Ministero della Salute Ricerca Finalizzata