Defects of Nutrient Signaling and Autophagy in Neurodegeneration.
AMPK
autophagy
glucose metabolism
lipid metabolism
mTORC1 (mechanistic target of rapamycin complex 1)
mitochondrial metabolism
neurodegenerative diseases
nutrient sensing pathways
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2022
2022
Historique:
received:
15
12
2021
accepted:
21
02
2022
entrez:
14
4
2022
pubmed:
15
4
2022
medline:
15
4
2022
Statut:
epublish
Résumé
Neurons are post-mitotic cells that allocate huge amounts of energy to the synthesis of new organelles and molecules, neurotransmission and to the maintenance of redox homeostasis. In neurons, autophagy is not only crucial to ensure organelle renewal but it is also essential to balance nutritional needs through the mobilization of internal energy stores. A delicate crosstalk between the pathways that sense nutritional status of the cell and the autophagic processes to recycle organelles and macronutrients is fundamental to guarantee the proper functioning of the neuron in times of energy scarcity. This review provides a detailed overview of the pathways and processes involved in the balance of cellular energy mediated by autophagy, which when defective, precipitate the neurodegenerative cascade of Parkinson's disease, frontotemporal dementia, amyotrophic lateral sclerosis or Alzheimer's disease.
Identifiants
pubmed: 35419363
doi: 10.3389/fcell.2022.836196
pii: 836196
pmc: PMC8996160
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
836196Informations de copyright
Copyright © 2022 Ondaro, Hernandez-Eguiazu, Garciandia-Arcelus, Loera-Valencia, Rodriguez-Gómez, Jiménez-Zúñiga, Goikolea, Rodriguez-Rodriguez, Ruiz-Martinez, Moreno, Lopez de Munain, Holt, Gil-Bea and Gereñu.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The handling editor declared a past co-authorship with one of the authors GG.
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