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HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases

High-mobility group box 1 (HMGB1) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation, and migration in eye diseases. It induces signaling pathways by binding to the receptor for advanced glycation end products (RAGE) and Toll-like receptors (TLRs) 2, 4,...

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Autores principales: Liu, Yi, Zhuang, Guo-Bin, Zhou, Xue-Zhi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6220384/
https://www.ncbi.nlm.nih.gov/pubmed/30473885
http://dx.doi.org/10.1155/2018/5195290
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author Liu, Yi
Zhuang, Guo-Bin
Zhou, Xue-Zhi
author_facet Liu, Yi
Zhuang, Guo-Bin
Zhou, Xue-Zhi
author_sort Liu, Yi
collection PubMed
description High-mobility group box 1 (HMGB1) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation, and migration in eye diseases. It induces signaling pathways by binding to the receptor for advanced glycation end products (RAGE) and Toll-like receptors (TLRs) 2, 4, and 9. This proinflammatory activity is considered to be important in the pathogenesis of a wide range of ocular diseases resulting from hemodynamic changes, presence of neovascular endothelial cells, secretion of intraocular immune factors or inflammation, and apoptosis of retinal cell layers. Further work is needed to elucidate in detail how HMGB1 contributes to ocular disease and how its damaging activity can be modulated. In this review, we summarize current knowledge on HMGB1 as a ligand that can evoke inflammation and immune responses in ocular diseases.
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spelling pubmed-62203842018-11-25 HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases Liu, Yi Zhuang, Guo-Bin Zhou, Xue-Zhi J Ophthalmol Review Article High-mobility group box 1 (HMGB1) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation, and migration in eye diseases. It induces signaling pathways by binding to the receptor for advanced glycation end products (RAGE) and Toll-like receptors (TLRs) 2, 4, and 9. This proinflammatory activity is considered to be important in the pathogenesis of a wide range of ocular diseases resulting from hemodynamic changes, presence of neovascular endothelial cells, secretion of intraocular immune factors or inflammation, and apoptosis of retinal cell layers. Further work is needed to elucidate in detail how HMGB1 contributes to ocular disease and how its damaging activity can be modulated. In this review, we summarize current knowledge on HMGB1 as a ligand that can evoke inflammation and immune responses in ocular diseases. Hindawi 2018-10-24 /pmc/articles/PMC6220384/ /pubmed/30473885 http://dx.doi.org/10.1155/2018/5195290 Text en Copyright © 2018 Yi Liu et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Liu, Yi
Zhuang, Guo-Bin
Zhou, Xue-Zhi
HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases
title HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases
title_full HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases
title_fullStr HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases
title_full_unstemmed HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases
title_short HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases
title_sort hmbg1 as a driver of inflammatory and immune processes in the pathogenesis of ocular diseases
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6220384/
https://www.ncbi.nlm.nih.gov/pubmed/30473885
http://dx.doi.org/10.1155/2018/5195290
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