Evidence map›Paper›PMID 20847143›Full record

ArticleJournal of the American Society of Nephrology : JASN2010

HMGB1 contributes to kidney ischemia reperfusion injury.

Huiling Wu, Jin Ma, Peng Wang, Theresa M Corpuz, Usha Panchapakesan, Kate R Wyburn, Steven J Chadban

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed, 2 pooled it
11.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

193 citing papers in PubMed, 2 syntheses or guidelines pooled it, 355 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The Protective Mechanism of Dexmedetomidine on Renal in Hemorrhagic Shock.Computational and mathematical methods in medicine · 2022
    Trial
  4. Plasma From Patients Undergoing Liver Transplantation Is Resistant to Anticoagulant Activity of Soluble Thrombomodulin.Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2019
    Trial
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  10. Transgenic expression of human CD47 on pig cells provides only partial protection against human macrophage-mediated destruction in human immune system mice.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026
    Article
  11. Article
  12. Enhanced Burn Wound Healing and Conversion Prevention Through Inhibition of High Mobility Group Box 1 in a Scald Burn Rat Model.Journal of burn care & research : official publication of the American Burn Association · 2026
    Article
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  14. Review
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133 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Huiling WuCollaborative Transplant Research Group, Royal Prince Alfred Hospital, Sydney, Australia. huiling.wu@sydney.edu.au
Jin Ma
Peng Wang
Theresa M Corpuz
Usha Panchapakesan
Kate R Wyburn
Steven J Chadban
Royal Prince Alfred Hospital · AUUniversity of Sydney · AURoyal North Shore Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-mobility group box 1 (HMGB1), a nuclear factor released extracellularly as an inflammatory cytokine, is an endogenous ligand for Toll-like receptor 4 (TLR4). TLR4 activation mediates kidney ischemia-reperfusion injury (IRI), but whether HMGB1 contributes to IRI is unknown. Here, treating wild-type mice with neutralizing anti-HMGB1 antibody protected them against kidney IRI, evidenced by lower serum creatinine and less tubular damage than untreated mice. Mice treated with anti-HMGB1 had significantly less tubulointerstitial infiltration by neutrophils (day 1) and macrophages (day 5) and markedly reduced apoptosis of tubular epithelial cells. Furthermore, anti-HMGB1 antibody-treated IRI kidneys had significantly lower levels of IL-6, TNFα, and monocyte chemoattractant protein 1 (MCP1). mRNA, which are downstream of HMGB1. Conversely, administration of rHMGB1 after reperfusion exacerbated kidney IRI in wild-type mice. TLR4 deficient (TLR4(-/-)) mice were protected against kidney IRI; administration of neither anti-HMGB1 antibody nor rHMGB1 affected this renoprotection. In conclusion, endogenous HMGB1 promotes kidney damage after IRI, possibly through the TLR4 pathway. Administration of a neutralizing antibody to HMGB1 either before or soon after ischemia-reperfusion affords significant protection, suggesting therapeutic potential for acute kidney injury.

Indexed as

Acute Kidney InjuryAnimalsAntibodies, Anti-IdiotypicApoptosisChemokine CCL2EpitheliumHMGB1 ProteinInterleukin-6Kidney TubulesMaleMiceMice, Inbred C57BLMice, KnockoutModels, AnimalReperfusion InjuryToll-Like Receptor 4Antibodies, Anti-IdiotypicChemokine CCL2HMGB1 ProteinInterleukin-6Tlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID20847143
PMCPMC3014003
OpenAlexW2140655321

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.