The functional role of HMGB1/TLR4/NF-KB signalling pathway in multiple sclerosis
Küçük Resim Yok
Tarih
2022
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Nova Science Publishers, Inc.
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Multiple 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.
Açıklama
Anahtar Kelimeler
HMGB1, Multiple sclerosis, Nuclear factor-Kappa B, Toll-like receptor-4
Kaynak
HMGB1: Functions, Inhibitors and Clinical Significance
WoS Q Değeri
Scopus Q Değeri
N/A
