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Molecular mechanisms involved in the protective actions of Selective Estrogen Receptor Modulators in brain cells

dc.contributor.authorBaez-Jurado E.
dc.contributor.authorRincón-Benavides M.A.
dc.contributor.authorHidalgo-Lanussa O.
dc.contributor.authorGuio-Vega G.
dc.contributor.authorAshraf G.M.
dc.contributor.authorSahebkar A.
dc.contributor.authorEcheverria V.
dc.contributor.authorGarcia-Segura L.M.
dc.contributor.authorBarreto G.E.
dc.date.accessioned2020-09-02T22:12:36Z
dc.date.available2020-09-02T22:12:36Z
dc.date.issued2019
dc.identifier10.1016/j.yfrne.2018.09.001
dc.identifier.citation52, , 44-64
dc.identifier.issn00913022
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3669
dc.descriptionSynthetic selective modulators of the estrogen receptors (SERMs) have shown to protect neurons and glial cells against toxic insults. Among the most relevant beneficial effects attributed to these compounds are the regulation of inflammation, attenuation of astrogliosis and microglial activation, prevention of excitotoxicity and as a consequence the reduction of neuronal cell death. Under pathological conditions, the mechanism of action of the SERMs involves the activation of estrogen receptors (ERs) and G protein-coupled receptor for estrogens (GRP30). These receptors trigger neuroprotective responses such as increasing the expression of antioxidants and the activation of kinase-mediated survival signaling pathways. Despite the advances in the knowledge of the pathways activated by the SERMs, their mechanism of action is still not entirely clear, and there are several controversies. In this review, we focused on the molecular pathways activated by SERMs in brain cells, mainly astrocytes, as a response to treatment with raloxifene and tamoxifen. © 2018 Elsevier Inc.
dc.language.isoen
dc.publisherAcademic Press Inc.
dc.subjectAstrocytes
dc.subjectBrain pathologies
dc.subjectEstrogen receptors
dc.subjectGRP30
dc.subjectSERMs
dc.subjectTamoxifen
dc.subjectafimoxifene
dc.subjectcre recombinase
dc.subjectdroloxifene
dc.subjectdrug metabolite
dc.subjectendoxifen
dc.subjectestrogen receptor
dc.subjectG protein coupled receptor 30
dc.subjecthydroxytamoxifen
dc.subjectinositol 1,4,5 trisphosphate receptor
dc.subjectinositol 1,4,5 trisphosphate receptor 2
dc.subjectNotch1 receptor
dc.subjectraloxifene
dc.subjectselective estrogen receptor modulator
dc.subjecttamoxifen
dc.subjectunclassified drug
dc.subjectestrogen receptor
dc.subjectneuroprotective agent
dc.subjectselective estrogen receptor modulator
dc.subjectastrocyte
dc.subjectbrain cell
dc.subjectbrain damage
dc.subjectcell differentiation
dc.subjectcell fate
dc.subjectcell function
dc.subjectcell interaction
dc.subjectcentral nervous system disease
dc.subjectdrug mechanism
dc.subjectdrug response
dc.subjecthuman
dc.subjectLoxP site
dc.subjectmemory
dc.subjectmicroglia
dc.subjectnerve cell
dc.subjectnervous system inflammation
dc.subjectneural stem cell
dc.subjectneuroprotection
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectReview
dc.subjectanimal
dc.subjectbrain disease
dc.subjectdrug effect
dc.subjectmetabolism
dc.subjectAnimals
dc.subjectAstrocytes
dc.subjectBrain Diseases
dc.subjectHumans
dc.subjectNeuroprotective Agents
dc.subjectRaloxifene Hydrochloride
dc.subjectReceptors, Estrogen
dc.subjectSelective Estrogen Receptor Modulators
dc.subjectTamoxifen
dc.titleMolecular mechanisms involved in the protective actions of Selective Estrogen Receptor Modulators in brain cells
dc.typeReview


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