The functional role of HMGB1/TLR4/NF-KB signalling pathway in multiple sclerosis

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dc.authorscopusid58016817800
dc.authorscopusid57189842131
dc.authorscopusid56005201400
dc.authorscopusid57151399700
dc.contributor.authorUluc, Firdevs
dc.contributor.authorBozat, Bihter Gokce
dc.contributor.authorKarabork, Seyda
dc.contributor.authorAydin-Turkoglu, Sule
dc.date.accessioned2024-09-25T19:45:27Z
dc.date.available2024-09-25T19:45:27Z
dc.date.issued2022
dc.departmentAbant İzzet Baysal Üniversitesien_US
dc.description.abstractMultiple sclerosis (MS) is a chronic autoimmune demyelinating disorder of the central nervous system (CNS) defined by features such as axonal loss, glial cell activation, and immune cell infiltration. To date, the molecular mechanism underlying inflammation and immune response in MS pathogenesis has not been fully understood. Elucidation of the existing pathogenic mechanism is crucial for the development of effective treatment options for this disease. High Mobility Group Box 1 (HMGB1) protein is a proinflammatory-like cytokine protein that has an initiating role in neuroinflammation in triggering MS. In recent years, HMGB1 and its related signaling pathways have become a therapeutic target in experimental and clinical MS studies. In particular, HMGB1/TLR4/ NF-?B signaling pathway has an increasing importance. The main goal of this chapter is to explain the effects of HMGB1/TLR4/NF-KB signaling pathway in MS pathophysiology, which enhancing the release of proinflammatory cytokines and causes an inflammatory response. In order to develop effective treatment strategies in MS in the future, this chapter aims to explain the mechanism of HMGB1-induced neuroinflammation. © 2023 by Nova Science Publishers, Inc. All rights reserved.en_US
dc.identifier.endpage238en_US
dc.identifier.isbn979-888697466-9
dc.identifier.isbn979-888697408-9
dc.identifier.scopus2-s2.0-85143993720en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage219en_US
dc.identifier.urihttps://hdl.handle.net/20.500.12491/13037
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherNova Science Publishers, Inc.en_US
dc.relation.ispartofHMGB1: Functions, Inhibitors and Clinical Significanceen_US
dc.relation.publicationcategoryKitap Bölümü - Uluslararasıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmzYK_20240925en_US
dc.subjectHMGB1en_US
dc.subjectMultiple sclerosisen_US
dc.subjectNuclear factor-Kappa Ben_US
dc.subjectToll-like receptor-4en_US
dc.titleThe functional role of HMGB1/TLR4/NF-KB signalling pathway in multiple sclerosisen_US
dc.typeBook Chapteren_US

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