CoChat
Sign Up
Cited by 956Advanced Glycation End Products researchImmune Response and InflammationHeat shock proteins research

The DOI matches its Crossref record; 1,872 of the 1,872 references it cites were found in a registry or an index.

HMGB1 in health and disease

Open access
Kang, Rui, Chen, Ruochan, Zhang, Qiuhong, Hou, Wen, Wu, Sha, Cao, Lizhi, Huang, Jin, Yu, Yan, Fan, Xue-gong, Yan, Zhengwen, Sun, Xiaofang, Wang, Haichao, Wang, Qingde, Tsung, Allan, Billiar, Timothy R., Zeh, Herbert J., Lotze, Michael T., Tang, Daolin·2014·Molecular Aspects of Medicine
DOI 10.1016/j.mam.2014.05.001PMC PMC4254084
Open this paper in CoChat — free account

Abstract

Complex genetic and physiological variations as well as environmental factors that drive emergence of chromosomal instability, development of unscheduled cell death, skewed differentiation, and altered metabolism are central to the pathogenesis of human diseases and disorders. Understanding the molecular bases for these processes is important for the development of new diagnostic biomarkers, and for identifying new therapeutic targets. In 1973, a group of non-histone nuclear proteins with high electrophoretic mobility was discovered and termed high-mobility group (HMG) proteins. The HMG proteins include three superfamilies termed HMGB, HMGN, and HMGA. High-mobility group box 1 (HMGB1), the most abundant and well-studied HMG protein, senses and coordinates the cellular stress response and plays a critical role not only inside of the cell as a DNA chaperone, chromosome guardian, autophagy sustainer, and protector from apoptotic cell death, but also outside the cell as the prototypic damage associated molecular pattern molecule (DAMP). This DAMP, in conjunction with other factors, thus has cytokine, chemokine, and growth factor activity, orchestrating the inflammatory and immune response. All of these characteristics make HMGB1 a critical molecular target in multiple human diseases including infectious diseases, ischemia, immune disorders, neurodegenerative diseases, metabolic disorders, and cancer. Indeed, a number of emergent strategies have been used to inhibit HMGB1 expression, release, and activity in vitro and in vivo. These include antibodies, peptide inhibitors, RNAi, anti-coagulants, endogenous hormones, various chemical compounds, HMGB1-receptor and signaling pathway inhibition, artificial DNAs, physical strategies including vagus nerve stimulation and other surgical approaches. Future work further investigating the details of HMGB1 localization, structure, post-translational modification, and identification of additional partners will undoubtedly uncover additional secrets regarding HMGB1's multiple functions.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.mam.2014.05.001

Cites

1872 of 1872 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

16 retracted

Items 1,401–1,600 of 1,872

Flagged first, then by citations

Research works printed but not linked: 27

  1. Antoine, 2012, Molecular forms of HMGB1 and keratin-18 as mechanistic biomarkers for mode of cell death and prognosis during clinical acetaminophen hepatotoxicity, J. Hepatol., 56, 1070, 10.1016/j.jhep.2011.12.019 · DOI
  2. Arends, 1990, Apoptosis. The role of the endonuclease, Am. J. Pathol., 136, 593
  3. Bamboat, 2009, Toll-like receptor 9 inhibition confers protection from liver ischemia–reperfusion injury, Hepatology
  4. Cavone, 2011, 18beta-glycyrrhetic acid inhibits immune activation triggered by HMGB1, a pro-inflammatory protein found in the tear fluid during conjunctivitis and blepharitis, Ocul. Immunol. Inflamm., 19, 180, 10.3109/09273948.2010.538121 · DOI
  5. Chiba, 2012, Tumor-infiltrating DCs suppress nucleic acid-mediated innate immune responses through interactions between the receptor TIM-3 and the alarmin HMGB1, Nat. Immunol., 13, 832, 10.1038/ni.2376 · DOI · Paper page
  6. de Souza, 2013, Is serum HMGB1 a biomarker in ANCA-associated vasculitis?, Arthritis Res. Ther., 15, R104, 10.1186/ar4284 · DOI
  7. Huang, 2013, Hepatocyte specific HMGB1 deletion worsens the injury in liver ischemia/reperfusion: a role for intracellular HMGB1 in cellular protection, Hepatology
  8. Kaczorowski, 2009, Innate immune mechanisms in ischemia/reperfusion, Front. Biosci. (Elite Ed.), 1, 91
  9. Kang, 2012, The expression of the receptor for advanced glycation endproducts (RAGE) is permissive for early pancreatic neoplasia, Proc. Natl. Acad. Sci. U.S.A., 10.1073/pnas.1113865109 · DOI · Paper page
  10. Kang, 2013, The HMGB1/RAGE inflammatory pathway promotes pancreatic tumor growth by regulating mitochondrial bioenergetics, Oncogene
  11. Krynetski, 2003, Cancer Res., 63, 100
  12. Liu, 2013, The fibrin-derived peptide Bss15-42 attenuates the liver damage in a rat model of liver ischemia reperfusion injury, Shock (Augusta, GA), 10
  13. Liu, 2011, HMGB1-induced autophagy promotes chemotherapy resistance in leukemia cells, Leukemia, 25, 23, 10.1038/leu.2010.225 · DOI
  14. Livesey, 2012, p53/HMGB1 complexes regulate autophagy and apoptosis, Cancer Res., 72, 1996, 10.1158/0008-5472.CAN-11-2291 · DOI
  15. Livesey, 2012, p53/HMGB1 complexes regulate autophagy and apoptosis, Cancer Res., 10.1158/0008-5472.CAN-11-2291 · DOI
  16. Lu, 2012, Novel role of PKR in inflammasome activation and HMGB1 release, Nature, 488, 670, 10.1038/nature11290 · DOI
  17. Maugeri, 2012, Circulating platelets as a source of the damage-associated molecular pattern HMGB1 in patients with systemic sclerosis, Autoimmunity, 10.3109/08916934.2012.719946 · DOI
  18. Morris, 2010, KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma, Nat. Rev. Cancer, 10, 683, 10.1038/nrc2899 · DOI
  19. Shi, 2012, Enhanced HMGB1 expression may contribute to Th17 cells activation in rheumatoid arthritis, Clin. Dev. Immunol., 2012, 295081, 10.1155/2012/295081 · DOI
  20. Tang, 2010, Endogenous HMGB1 regulates autophagy, J. Cell Biol., 190, 881, 10.1083/jcb.200911078 · DOI · Paper page
  21. van Beijnum, 2012, Tumor angiogenesis is enforced by autocrine regulation of high-mobility group box 1, Oncogene
  22. Wang, 2013, Redox-sensitive structural change in the A-domain of HMGB1 and its implication for the binding to cisplatin modified DNA, Biochem. Biophys. Res. Commun., 10.1016/j.bbrc.2013.10.085 · DOI
  23. Wang, 2014, Inhibition of high-mobility group box 1 improves myocardial fibrosis and dysfunction in diabetic cardiomyopathy, Int. J. Cardiol.
  24. Wang, 2013, High-mobility group box 1 (HMGB1)-toll-like receptor (TLR)4-interleukin (IL)-23-IL-17A axis in drug-induced damage-associated lethal hepatitis: Interaction of gamma delta T cells with macrophages, Hepatology, 57, 373, 10.1002/hep.25982 · DOI
  25. Yamamoto, 2010, Hemoperfusion with a high-mobility group box 1 adsorption column can prevent the occurrence of hepatic ischemia–reperfusion injury in rats, Crit. Care Med., 38, 879, 10.1097/CCM.0b013e3181c58951 · DOI
  26. Yao, 2009, Hyperglycemia-induced reactive oxygen species increase expression of RAGE and RAGE ligands, Diabetes
  27. Zhou, 2011, HMGB1 cytoplasmic translocation in patients with acute liver failure, BMC Gastroenterol., 11, 10.1186/1471-230X-11-21 · DOI

Cited by

Sorted by citations

See all 956

Related

See all

Metadata

Authors
Kang, R., Chen, R., Zhang, Q., Hou, W., Wu, S., Cao, L., Huang, J., Yu, Y., Fan, X.-G., Yan, Z., Sun, X., Wang, H., Wang, Q., Tsung, A., Billiar, T. R., Zeh, H. J., Lotze, M. T., & Tang, D.
Affiliations
  • University of Pittsburgh (US)
  • Central South University (CN)
  • Sun Yat-sen University (CN)
  • Third Affiliated Hospital of Guangzhou Medical University (CN)
  • Feinstein Institute for Medical Research (US)
Corresponding author
  • Kang, Rui
  • Tang, Daolin
ORCID
Venue
Molecular Aspects of Medicine
Publisher
Elsevier BV
Published
2014-12
Volume
40
Pages
1-116
ISSN
0098-2997 (ISSN-L)
DOI
10.1016/j.mam.2014.05.001
PMC
PMC4254084
OpenAlex
W2075035271
Cited by
956
References
1,872
Citations by year
2026: 33 · 2025: 64 · 2024: 80 · 2023: 87 · 2022: 119 · 2021: 113 · 2020: 114 · 2019: 83 · 2018: 88 · 2017: 53 · 2016: 67 · 2015: 45 · 2014: 8
FWCI
7.41
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Molecular Aspects of Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (R01CA160417, R01CA181450, R01AT005076, R01GM063075)
  • National Natural Sciences Foundation of China (31171328)
  • 2013 Pancreatic Cancer Action Network–AACR Career Development Award (13-20-25-TANG)
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 › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
Keywords
HMGB1, high mobility group box 1, high mobility group proteins, chromosomal instability, DNA damage response, autophagy, apoptosis, damage-associated molecular patterns, inflammation, immune response, HMGB1 inhibitors, neurodegenerative diseases, cancer, ischemia, post-translational modification
MeSH terms
Disease, Health, Humans, HMGB1 Protein

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review