Cited by 762Advanced Glycation End Products researchImmune Response and InflammationBiomarkers in Disease Mechanisms

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HMGB1: Endogenous Danger Signaling

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Klune, John R., Dhupar, Rajeev, Cardinal, Jon, Billiar, Timothy R., Tsung, Allan·2008·Molecular Medicine

DOI 10.2119/2008-00034.klunePMC PMC2323334

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Abstract

While foreign pathogens and their products have long been known to activate the innate immune system, the recent recognition of a group of endogenous molecules that serve a similar function has provided a framework for understanding the overlap between the inflammatory responses activated by pathogens and injury. These endogenous molecules, termed alarmins, are normal cell constituents that can be released into the extracellular milieu during states of cellular stress or damage and subsequently activate the immune system. One nuclear protein, High mobility group box-1 (HMGB1), has received particular attention as fulfilling the functions of an alarmin by being involved in both infectious and non-infectious inflammatory conditions. Once released, HMGB1 signals through various receptors to activate immune cells involved in the immune process. Although initial studies demonstrated HMGB1 as a late mediator of sepsis, recent findings indicate HMGB1 to have an important role in models of non-infectious inflammation, such as autoimmunity, cancer, trauma, and ischemia reperfusion injury. Furthermore, in contrast to its pro-inflammatory functions, there is evidence that HMGB1 also has restorative effects leading to tissue repair and regeneration. The complex functions of HMGB1 as an archetypical alarmin are outlined here to review our current understanding of a molecule that holds the potential for treatment in many important human conditions.

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Authors: Klune, J. R., Dhupar, R., Cardinal, J., Billiar, T. R., & Tsung, A.
Affiliations: University of Pittsburgh (US)
Corresponding author: Tsung, Allan
ORCID: Klune, John R.
Dhupar, Rajeev
Billiar, Timothy R.
Tsung, Allan
Venue: Molecular Medicine
Publisher: Springer Science and Business Media LLC
Published: 2008-04-11
Volume: 14
Issue: 7-8
Pages: 476-484
ISSN: 1076-1551 (ISSN-L)
1528-3658
DOI: 10.2119/2008-00034.klune
PMC: PMC2323334
OpenAlex: W168035116
Cited by: 762
References: 129
Citations by year: 2026: 14 · 2025: 15 · 2024: 29 · 2023: 32 · 2022: 35 · 2021: 47 · 2020: 53 · 2019: 53 · 2018: 48 · 2017: 44 · 2016: 45 · 2015: 55 · 2014: 54 · 2013: 48 · 2012: 45
FWCI: 6.58
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
Locations: Molecular Medicine (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
Keywords: HMGB1, alarmins, danger signaling, innate immunity, inflammation, sepsis, autoimmunity, cancer, trauma (physical injury), ischemia-reperfusion injury, tissue repair, regeneration
MeSH terms: Receptor for Advanced Glycation End Products, Animals, Cell Nucleus, Disease, Humans, Immunity, Innate, Models, Biological, Receptors, Immunologic, Regeneration, Signal Transduction, Inflammation Mediators, HMGB1 Protein, Toll-Like Receptors

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HMGB1: Endogenous Danger Signaling

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