Protective function of autophagy during VLCFA-induced cytotoxicity in a neurodegenerative cell model.
Fiche publication
Date publication
avril 2019
Journal
Free radical biology & medicine
Auteurs
Membres identifiés du Cancéropôle Est :
Pr DELMAS Dominique, Dr LIZARD Gérard
Tous les auteurs :
Doria M, Nury T, Delmas D, Moreau T, Lizard G, Vejux A
Lien Pubmed
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.
Mots clés
Autophagy, Lipotoxicity, Neurodegenerative diseases, Oxidative stress, Rapamycin, Very long chain fatty acid
Référence
Free Radic. Biol. Med.. 2019 Apr 17;: