Enlightening the role of high mobility group box 1 (HMGB1) in inflammation: Updates on receptor signalling

Paudel YN 1 , Angelopoulou E 2 , Piperi C 3 , Balasubramaniam VRMT 4 , Othman I 5 , Shaikh MF 6

Affiliations 

  • 1 Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor, Malaysia. Electronic address: yam.paudel@monash.edu
  • 2 Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, Athens, Greece. Electronic address: angelthal@med.uoa.gr
  • 3 Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, Athens, Greece. Electronic address: cpiperi@med.uoa.gr
  • 4 Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor, Malaysia. Electronic address: vinod.balasubramaniam@monash.edu
  • 5 Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor, Malaysia. Electronic address: iekhsan.othman@monash.edu
  • 6 Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor, Malaysia. Electronic address: farooq.shaikh@monash.edu
Eur J Pharmacol, 2019 Sep 05;858:172487.
PMID: 31229535 DOI: 10.1016/j.ejphar.2019.172487

Abstract

High mobility group box 1 (HMGB1) is a ubiquitous protein, released passively by necrotic tissues or secreted actively by stressed cells. Extracellular HMGB1 is a typical damage-associated molecular pattern (DAMP) molecule which generates different redox types through binding with several receptors and signalling molecules, aggravating a range of cellular responses, including inflammation. HMGB1 is reported to participate in the pathogenesis of inflammatory diseases, through the interaction with pivotal transmembrane receptors, including the receptor for advanced glycation end products (RAGE) and toll-like receptor-4 (TLR-4). This review aims to highlight the role of HMGB1 in the innate inflammatory response describing its interaction with several cofactors and receptors that coordinate its downstream effects. Novel and underexplored HMGB1 binding molecules that have been actively involved in HMGB1-mediated inflammatory diseases/conditions with therapeutic potential are further discussed.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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