Endogenous Ligands of TLR4 in Microglia: Potential Targets for Related Neurological Diseases.
HMGB1
S100A8/A9
TLR4
fetuin-A.
heme
microglia
neuroinflammatory diseases
Journal
Current drug targets
ISSN: 1873-5592
Titre abrégé: Curr Drug Targets
Pays: United Arab Emirates
ID NLM: 100960531
Informations de publication
Date de publication:
04 Sep 2024
04 Sep 2024
Historique:
received:
08
04
2024
revised:
09
07
2024
accepted:
30
07
2024
medline:
5
9
2024
pubmed:
5
9
2024
entrez:
5
9
2024
Statut:
aheadofprint
Résumé
Chronic inflammation mediated by microglia is a cause of some neuroinflammatory diseases. TLR4, a natural immune receptor on microglia, plays an important role in the occurrence of inflammation and the process of diseases. TLR4 can be activated by a variety of ligands to trigger inflammatory responses, including endogenous ligands HMGB1, S100A8/9, Heme, and Fetuin-A. As ligands derived from the body itself, they have the ability to bind directly to TLR4 and can be used as inducers of aseptic inflammation. In the past 20 years, targeting ligands rather than receptors has become an emerging therapeutic strategy for the treatment of diseases, so understanding the relationship between microglia, TLR4, TLR4 ligands, and corresponding diseases may have new implications for the treatment of diseases. In the article, we will discuss the TLR4 and the endogenous substances that can activate the TLR4 signaling pathway and present literature support for their role in neuroinflammatory diseases.
Identifiants
pubmed: 39234911
pii: CDT-EPUB-142797
doi: 10.2174/0113894501316051240821060249
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
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