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Metabolic and Inflammatory Adaptation of Reactive Astrocytes: Role of PPARs

dc.contributor.authorIglesias J.
dc.contributor.authorMorales L.
dc.contributor.authorBarreto G.E.
dc.date.accessioned2020-09-02T22:20:35Z
dc.date.available2020-09-02T22:20:35Z
dc.date.issued2017
dc.identifier10.1007/s12035-016-9833-2
dc.identifier.citation54, 4, 2518-2538
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4928
dc.descriptionAstrocyte-mediated inflammation is associated with degenerative pathologies such as Alzheimer’s and Parkinson’s diseases and multiple sclerosis. The acute inflammation and morphological and metabolic changes that astrocytes develop after the insult are known as reactive astroglia or astrogliosis that is an important response to protect and repair the lesion. Astrocytes optimize their metabolism to produce lactate, glutamate, and ketone bodies in order to provide energy to the neurons that are deprived of nutrients upon insult. Firstly, we review the basis of inflammation and morphological changes of the different cell population implicated in reactive gliosis. Next, we discuss the more active metabolic pathways in healthy astrocytes and explain the metabolic response of astrocytes to the insult in different pathologies and which metabolic alterations generate complications in these diseases. We emphasize the role of peroxisome proliferator-activated receptors isotypes in the inflammatory and metabolic adaptation of astrogliosis developed in ischemia or neurodegenerative diseases. Based on results reported in astrocytes and other cells, we resume and hypothesize the effect of peroxisome proliferator-activated receptor (PPAR) activation with ligands on different metabolic pathways in order to supply energy to the neurons. The activation of selective PPAR isotype activity may serve as an input to better understand the role played by these receptors on the metabolic and inflammatory compensation of astrogliosis and might represent an opportunity to develop new therapeutic strategies against traumatic brain injuries and neurodegenerative diseases. © 2016, Springer Science+Business Media New York.
dc.language.isoen
dc.publisherHumana Press Inc.
dc.subjectAstrogliosis
dc.subjectFatty acid oxidation
dc.subjectGlutamate
dc.subjectGlycolysis
dc.subjectKetone bodies
dc.subjectNeuroprotection
dc.subjectPPAR
dc.subjectglucose
dc.subjectglutamic acid
dc.subjectglutamine
dc.subjectlactic acid
dc.subjectperoxisome proliferator activated receptor
dc.subjectperoxisome proliferator activated receptor alpha
dc.subjectperoxisome proliferator activated receptor delta
dc.subjectperoxisome proliferator activated receptor gamma
dc.subjectperoxisome proliferator activated receptor
dc.subjectastrocyte
dc.subjectastrocytosis
dc.subjectcell interaction
dc.subjectcell metabolism
dc.subjectcell structure
dc.subjectdegenerative disease
dc.subjectfatty acid metabolism
dc.subjectgliosis
dc.subjectglutamate glutamine cycle
dc.subjecthuman
dc.subjectischemia
dc.subjectmacroglia
dc.subjectmicroglia
dc.subjectmodulation
dc.subjectnervous system inflammation
dc.subjectnonhuman
dc.subjectprotein function
dc.subjectReview
dc.subjectanimal
dc.subjectastrocyte
dc.subjectbiological model
dc.subjectgliosis
dc.subjectinflammation
dc.subjectmetabolism
dc.subjectpathology
dc.subjectAnimals
dc.subjectAstrocytes
dc.subjectGliosis
dc.subjectHumans
dc.subjectInflammation
dc.subjectModels, Biological
dc.subjectPeroxisome Proliferator-Activated Receptors
dc.titleMetabolic and Inflammatory Adaptation of Reactive Astrocytes: Role of PPARs
dc.typeReview


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