Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024;25(14):953-970.
doi: 10.2174/0113894501316051240821060249.

Endogenous Ligands of TLR4 in Microglia: Potential Targets for Related Neurological Diseases

Bo Chen  1   2 , Bin Di  1   2
Affiliations
Review

Endogenous Ligands of TLR4 in Microglia: Potential Targets for Related Neurological Diseases

Bo Chen et al. Curr Drug Targets. 2024.

Abstract

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.

Keywords: Fetuin-A.; HMGB1; Heme; S100A8/A9; TLR4; microglia; neuroinflammatory diseases.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

References

    1. A current view on inflammation. Nat Immunol 2017,18(8),825 - DOI - PubMed
    1. Medzhitov R.; Inflammation 2010: New adventures of an old flame. Cell 2010,140(6),771-776 - DOI - PubMed
    1. Castanheira F.V.S.; Kubes P.; Neutrophils and NETs in modulating acute and chronic inflammation. Blood 2019,133(20),2178-2185 - DOI - PubMed
    1. Hannoodee S.; Nasuruddin D.N.; Acute inflammatory response. StatPearls 2023 - PubMed
    1. Chen L.; Deng H.; Cui H.; Fang J.; Zuo Z.; Deng J.; Li Y.; Wang X.; Zhao L.; Inflammatory responses and inflammation-associated diseases in organs. Oncotarget 2018,9(6),7204-7218 - DOI - PubMed

MeSH terms

LinkOut - more resources