Protective function of autophagy during VLCFA-induced cytotoxicity in a neurodegenerative cell model.
Animals
Autophagy
/ physiology
Brain
/ pathology
Cell Death
Cells, Cultured
Fatty Acids
/ metabolism
Fibroblasts
/ physiology
Humans
Mice
Mice, Inbred BALB C
Neurodegenerative Diseases
/ metabolism
Neurons
/ physiology
Oligodendroglia
/ physiology
Oxidative Stress
Reactive Oxygen Species
/ metabolism
Autophagy
Lipotoxicity
Neurodegenerative diseases
Oxidative stress
Rapamycin
Very long chain fatty acid
Journal
Free radical biology & medicine
ISSN: 1873-4596
Titre abrégé: Free Radic Biol Med
Pays: United States
ID NLM: 8709159
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
11
03
2019
revised:
12
04
2019
accepted:
13
04
2019
pubmed:
21
4
2019
medline:
9
6
2020
entrez:
21
4
2019
Statut:
ppublish
Résumé
In recent years, a particular interest has focused on the accumulation of fatty acids with very long chains (VLCFA) in the occurrence of neurodegenerative diseases such as Alzheimer's disease, multiple sclerosis or dementia. Indeed, it seems increasingly clear that this accumulation of VLCFA in the central nervous system is accompanied by a progressive demyelination resulting in death of neuronal cells. Nevertheless, molecular mechanisms by which VLCFA result in toxicity remain unclear. This study highlights for the first time in 3 different cellular models (oligodendrocytes 158 N, primary mouse brain culture, and patient fibroblasts) the types of cell death involved where VLCFA-induced ROS production leads to autophagy. The autophagic process protects the cell from this VLCFA-induced toxicity. Thus, autophagy in addition to oxidative stress can offer new therapeutic approaches.
Identifiants
pubmed: 31004752
pii: S0891-5849(19)30413-7
doi: 10.1016/j.freeradbiomed.2019.04.016
pii:
doi:
Substances chimiques
Fatty Acids
0
Reactive Oxygen Species
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
46-58Informations de copyright
Copyright © 2019. Published by Elsevier Inc.