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Astrocytes and endoplasmic reticulum stress: A bridge between obesity and neurodegenerative diseases

dc.contributor.authorMartin-Jiménez C.A.
dc.contributor.authorGarcía-Vega Á.
dc.contributor.authorCabezas R.
dc.contributor.authorAliev G.
dc.contributor.authorEcheverria V.
dc.contributor.authorGonzález J.
dc.contributor.authorBarreto G.E.
dc.date.accessioned2020-09-02T22:22:22Z
dc.date.available2020-09-02T22:22:22Z
dc.date.issued2017
dc.identifier10.1016/j.pneurobio.2017.08.001
dc.identifier.citation158, , 45-68
dc.identifier.issn03010082
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5211
dc.descriptionEndoplasmic reticulum (ER) is a subcellular organelle involved in protein folding and processing. ER stress constitutes a cellular process characterized by accumulation of misfolded proteins, impaired lipid metabolism and induction of inflammatory responses. ER stress has been suggested to be involved in several human pathologies, including neurodegenerative diseases and obesity. Different studies have shown that both neurodegenerative diseases and obesity trigger similar cellular responses to ER stress. Moreover, both diseases are assessed in astrocytes as evidences suggest these cells as key regulators of brain homeostasis. However, the exact contributions to the effects of ER stress in astrocytes in the various neurodegenerative diseases and its relation with obesity are not well known. Here, we discuss recent advances in the understanding of molecular mechanisms that regulate ER stress-related disorders in astrocytes such as obesity and neurodegeneration. Moreover, we outline the correlation between the activated proteins of the unfolded protein response (UPR) in these pathological conditions in order to identify possible therapeutic targets for ER stress in astrocytes. We show that ER stress in astrocytes shares UPR activation pathways during both obesity and neurodegenerative diseases, demonstrating that UPR related proteins like ER chaperone GRP 78/Bip, PERK pathway and other exogenous molecules ameliorate UPR response and promote neuroprotection. © 2017 Elsevier Ltd
dc.language.isoen
dc.publisherElsevier Ltd
dc.subjectAstrocytes
dc.subjectEndoplasmic reticulum
dc.subjectER stress
dc.subjectNeurodegenerative diseases
dc.subjectObesity
dc.subjectactivating transcription factor 6
dc.subjectglucose regulated protein 78
dc.subjectprotein IRE1
dc.subjectAlzheimer disease
dc.subjectamyotrophic lateral sclerosis
dc.subjectastrocyte
dc.subjectautophosphorylation
dc.subjectbrain
dc.subjectdegenerative disease
dc.subjectendoplasmic reticulum associated degradation
dc.subjectendoplasmic reticulum stress
dc.subjectenzyme phosphorylation
dc.subjecthomeostasis
dc.subjecthuman
dc.subjectintracellular signaling
dc.subjectlipid metabolism
dc.subjectmolecule
dc.subjectneuroprotection
dc.subjectnonhuman
dc.subjectobesity
dc.subjectParkinson disease
dc.subjectpriority journal
dc.subjectprotein aggregation
dc.subjectprotein folding
dc.subjectReview
dc.subjectunfolded protein response
dc.subjectanimal
dc.subjectastrocyte
dc.subjectdegenerative disease
dc.subjectendoplasmic reticulum stress
dc.subjectmetabolism
dc.subjectobesity
dc.subjectpathophysiology
dc.subjectphysiology
dc.subjectAnimals
dc.subjectAstrocytes
dc.subjectEndoplasmic Reticulum Stress
dc.subjectHumans
dc.subjectNeurodegenerative Diseases
dc.subjectObesity
dc.titleAstrocytes and endoplasmic reticulum stress: A bridge between obesity and neurodegenerative diseases
dc.typeReview


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