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RESEARCH PRODUCT
Protective function of autophagy during VLCFA-induced cytotoxicity in a neurodegenerative cell model
Anne VejuxAnne VejuxGérard LizardThomas NuryMargaux DoriaThibault MoreauDominique Delmassubject
0301 basic medicineProgrammed cell deathendocrine system diseases[SDV]Life Sciences [q-bio]Very long chain fatty acidCellCentral nervous systemBiologymedicine.disease_causeBiochemistry03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinePhysiology (medical)medicineAutophagyAnimalsHumansCells CulturedNeuronsMice Inbred BALB CCell DeathMultiple sclerosisAutophagyFatty AcidsBrainNeurodegenerative DiseasesFibroblastsmedicine.disease3. Good healthCell biologyOligodendrogliaOxidative Stress030104 developmental biologymedicine.anatomical_structurechemistryLipotoxicityReactive Oxygen Species030217 neurology & neurosurgeryOxidative stressdescription
Abstract 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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2019-06-30 |