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Rocchi, A.* ; Carminati, E.* ; De Fusco, A.* ; Kowalska, J.A.* ; Floss, T. ; Benfenati, F.*

REST/NRSF deficiency impairs autophagy and leads to cellular senescence in neurons.

Aging Cell, DOI: 10.1111/acel.13471:e13471 (2021)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Autophagy ; Mitochondria ; Neurons ; Oxidative Stress ; Rapamycin ; Rest/nrsf ; Senescence ; Trehalose; Rest; Abnormalities; Activation; Features
Sprache englisch
Veröffentlichungsjahr 2021
HGF-Berichtsjahr 2021
ISSN (print) / ISBN 1474-9718
e-ISSN 1474-9726
Zeitschrift Aging Cell
Quellenangaben Band: , Heft: , Seiten: , Artikelnummer: e13471 Supplement: ,
Verlag Wiley
Verlagsort 111 River St, Hoboken 07030-5774, Nj Usa
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Developmental Genetics (IDG)
POF Topic(s) 30204 - Cell Programming and Repair
Forschungsfeld(er) Genetics and Epidemiology
PSP-Element(e) G-500500-001
Förderungen Compagnia di San Paolo Torino
Ministero Istruzione, Universita e Ricerca
Ministero della Salute Ricerca Finalizzata
DOI 10.1111/acel.13471
WOS ID WOS:000695631100001
Scopus ID 85114795523
PubMed ID 34520100
Erfassungsdatum 2021-10-11
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