Envisioning the role of inwardly rectifying potassium (Kir) channel in epilepsy

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dc.authorid0000-0002-3942-2097
dc.authorscopusid57200989999
dc.authorscopusid57222640358
dc.authorscopusid57216899438
dc.authorscopusid57190245158
dc.authorscopusid57193202574
dc.authorwosidAKYUZ, Enes/W-7801-2018
dc.contributor.authorAkyüz, Enes
dc.contributor.authorKöklü, Betül
dc.contributor.authorÜner, Arda Kaan
dc.contributor.authorAngelopoulou, Efthalia
dc.contributor.authorPaudel, Yam Nath
dc.date.accessioned2022-05-11T14:48:28Z
dc.date.available2022-05-11T14:48:28Z
dc.date.issued2022
dc.departmentTekirdağ Namık Kemal Üniversitesi
dc.description.abstractEpilepsy is a devastating neurological disorder characterized by recurrent seizures attributed to the disruption of the dynamic excitatory and inhibitory balance in the brain. Epilepsy has emerged as a global health concern affecting about 70 million people worldwide. Despite recent advances in pre-clinical and clinical research, its etiopathogenesis remains obscure, and there are still no treatment strategies modifying disease progression. Although the precise molecular mechanisms underlying epileptogenesis have not been clarified yet, the role of ion channels as regulators of cellular excitability has increasingly gained attention. In this regard, emerging evidence highlights the potential implication of inwardly rectifying potassium (Kir) channels in epileptogenesis. Kir channels consist of seven different subfamilies (Kir1-Kir7), and they are highly expressed in both neuronal and glial cells in the central nervous system. These channels control the cell volume and excitability. In this review, we discuss preclinical and clinical evidence on the role of the several subfamilies of Kir channels in epileptogenesis, aiming to shed more light on the pathogenesis of this disorder and pave the way for future novel therapeutic approaches.
dc.description.sponsorshipMonash University MalaysiaMonash University
dc.description.sponsorshipYNP acknowledge Monash University Malaysia for awarding him with HDR scholarship.
dc.identifier.doi10.1002/jnr.24985
dc.identifier.endpage443
dc.identifier.issn0360-4012
dc.identifier.issn1097-4547
dc.identifier.issue2en_US
dc.identifier.pmid34713909
dc.identifier.scopus2-s2.0-85118227193
dc.identifier.scopusqualityQ2
dc.identifier.startpage413
dc.identifier.urihttps://doi.org/10.1002/jnr.24985
dc.identifier.urihttps://hdl.handle.net/20.500.11776/10647
dc.identifier.volume100
dc.identifier.wosWOS:000712358900001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorKöklü, Betül
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofJournal of Neuroscience Research
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectabnormal discharge
dc.subjecthyperexcitability
dc.subjectKir channels
dc.subjectseizure
dc.subjectTemporal-Lobe Epilepsy
dc.subjectKcnj10 Gene Polymorphisms
dc.subjectRectifier K+ Channels
dc.subjectGyrus Granule Cells
dc.subjectTs65dn Mouse Model
dc.subjectGain-Of-Function
dc.subjectGirk Channels
dc.subjectMaximal Electroshock
dc.subjectFunctional-Characterization
dc.subjectAltered Expression
dc.titleEnvisioning the role of inwardly rectifying potassium (Kir) channel in epilepsy
dc.typeReview Article

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