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Role of c-jun N-terminal kinases (JNKs) in epilepsy and metabolic cognitive impairment

dc.contributor.authorBusquets O.
dc.contributor.authorEttcheto M.
dc.contributor.authorCano A.
dc.contributor.authorManzine P.R.
dc.contributor.authorSánchez-Lopez E.
dc.contributor.authorEspinosa-Jiménez T.
dc.contributor.authorVerdaguer E.
dc.contributor.authorCastro-Torres R.D.
dc.contributor.authorBeas-Zarate C.
dc.contributor.authorSureda F.X.
dc.contributor.authorOlloquequi J.
dc.contributor.authorAuladell C.
dc.contributor.authorFolch J.
dc.contributor.authorCamins A.
dc.date.accessioned2020-09-02T22:13:36Z
dc.date.available2020-09-02T22:13:36Z
dc.date.issued2020
dc.identifier10.3390/ijms21010255
dc.identifier.citation21, 1, -
dc.identifier.issn16616596
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3808
dc.descriptionPrevious studies have reported that the regulatory function of the different c-Jun N-terminal kinases isoforms (JNK1, JNK2, and JNK3) play an essential role in neurological disorders, such as epilepsy and metabolic-cognitive alterations. Accordingly, JNKs have emerged as suitable therapeutic strategies. In fact, it has been demonstrated that some unspecific JNK inhibitors exert antidiabetic and neuroprotective effects, albeit they usually show high toxicity or lack therapeutic value. In this sense, natural specific JNK inhibitors, such as Licochalcone A, are promising candidates. Nonetheless, research on the understanding of the role of each of the JNKs remains mandatory in order to progress on the identification of new selective JNK isoform inhibitors. In the present review, a summary on the current gathered data on the role of JNKs in pathology is presented, as well as a discussion on their potential role in pathologies like epilepsy and metabolic-cognitive injury. Moreover, data on the effects of synthetic small molecule inhibitors that modulate JNK-dependent pathways in the brain and peripheral tissues is reviewed. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
dc.language.isoen
dc.publisherMDPI AG
dc.subjectBrain
dc.subjectC-Jun-N-terminal kinase
dc.subjectCognitive impairment
dc.subjectEpilepsy
dc.subjectJNK inhibitor
dc.subjectMetabolism
dc.subjectType 2 diabetes
dc.subjectactivating transcription factor 6
dc.subjectBIM protein
dc.subjectcytochrome c
dc.subjectcytochrome P450
dc.subjectglucose regulated protein 78
dc.subjectglutathione peroxidase
dc.subjectgrowth arrest and DNA damage inducible protein 153
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinsulin
dc.subjectinterleukin 1beta
dc.subjectisoenzyme
dc.subjectlicochalcone A
dc.subjectmitogen activated protein kinase
dc.subjectmitogen activated protein kinase 1
dc.subjectmitogen activated protein kinase 3
dc.subjectmitogen activated protein kinase 7
dc.subjectmitogen activated protein kinase p38
dc.subjectperoxiredoxin
dc.subjectprotein Bax
dc.subjectprotein bcl 2
dc.subjectprotein bcl xl
dc.subjectprotein c jun
dc.subjectprotein tyrosine phosphatase 1B
dc.subjectproton transporting adenosine triphosphate synthase
dc.subjectreactive oxygen metabolite
dc.subjectsecond mitochondrial activator of caspase
dc.subjectstress activated protein kinase
dc.subjectstress activated protein kinase inhibitor
dc.subjecttumor necrosis factor receptor associated factor 2
dc.subjectunindexed drug
dc.subjectantidiabetic agent
dc.subjectisoprotein
dc.subjectmitogen activated protein kinase
dc.subjectneuroprotective agent
dc.subjectstress activated protein kinase
dc.subjectapoptosis
dc.subjectautophagy (cellular)
dc.subjectcell cycle progression
dc.subjectcell death
dc.subjectcell proliferation
dc.subjectcell respiration
dc.subjectcitric acid cycle
dc.subjectcognitive defect
dc.subjectdementia
dc.subjectdentate gyrus
dc.subjectdisease course
dc.subjectdyslipidemia
dc.subjectendoplasmic reticulum stress
dc.subjectepilepsy
dc.subjectepileptogenesis
dc.subjecthuman
dc.subjecthyperinsulinemia
dc.subjectin situ hybridization
dc.subjectinsulin resistance
dc.subjectmetabolic syndrome X
dc.subjectnerve degeneration
dc.subjectneuroprotection
dc.subjectnon insulin dependent diabetes mellitus
dc.subjectnonhuman
dc.subjectobesity
dc.subjectoxidative phosphorylation
dc.subjectoxidative stress
dc.subjectprotein degradation
dc.subjectprotein phosphorylation
dc.subjectReview
dc.subjectseizure
dc.subjecttemporal lobe epilepsy
dc.subjectunfolded protein response
dc.subjectupregulation
dc.subjectanimal
dc.subjectbrain
dc.subjectcognitive defect
dc.subjectdrug effect
dc.subjectepilepsy
dc.subjectMAPK signaling
dc.subjectmetabolism
dc.subjectmitochondrion
dc.subjectpathology
dc.subjectphysiology
dc.subjectAnimals
dc.subjectBrain
dc.subjectCognitive Dysfunction
dc.subjectDiabetes Mellitus, Type 2
dc.subjectEndoplasmic Reticulum Stress
dc.subjectEpilepsy
dc.subjectHumans
dc.subjectHypoglycemic Agents
dc.subjectJNK Mitogen-Activated Protein Kinases
dc.subjectMAP Kinase Signaling System
dc.subjectMitochondria
dc.subjectMitogen-Activated Protein Kinases
dc.subjectNeuroprotective Agents
dc.subjectProtein Isoforms
dc.titleRole of c-jun N-terminal kinases (JNKs) in epilepsy and metabolic cognitive impairment
dc.typeReview


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