Evidence map›Paper›PMID 37989401›Full record

ArticleJournal of hepatology2024

Redox-sensitive high-mobility group box-1 isoforms contribute to liver fibrosis progression and resolution in mice.

Xiaodong Ge, Romain Desert, Fernando Magdaleno, Hui Han, Zhuolun Song, Sukanta Das, Dipti Athavale, Wei Chen, Ines Barahona, Daniel Lantvit and 3 more

Open access · greenAbstract read
In one paragraph

Article in Journal of hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Cysteine thiol-to-sulfonate oxidation induces unfolding for the functional switching of the extracellular HMGB1 protein.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
  4. Serum HMGB1 and Alcohol-Related Liver Disease.Journal of clinical medicine · 2026
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. [Analysis of serum lipidomics for a spontaneous hepatic fibrosis mouse model].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Article
  11. Review
  12. HMGB1: key mediator in digestive system diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  13. Article
  14. Oxidized HMGB1 Adducts Unleash Inflammation in Alcohol-Associated Liver Disease.Cellular and molecular gastroenterology and hepatology · 2024
    Article
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

13 authors at 2 institutions in 1 country.

Xiaodong GeDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St, suite 130 CSN, MC 847, Chicago, IL 60612, USA.
Romain DesertDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St, suite 130 CSN, MC 847, Chicago, IL 60612, USA.
Fernando MagdalenoDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St, suite 130 CSN, MC 847, Chicago, IL 60612, USA.
Hui HanDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St, suite 130 CSN, MC 847, Chicago, IL 60612, USA.
Zhuolun SongDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St, suite 130 CSN, MC 847, Chicago, IL 60612, USA.
Sukanta DasDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St, suite 130 CSN, MC 847, Chicago, IL 60612, USA.
Dipti AthavaleDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St, suite 130 CSN, MC 847, Chicago, IL 60612, USA.
Wei ChenDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St, suite 130 CSN, MC 847, Chicago, IL 60612, USA.
Ines BarahonaDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St, suite 130 CSN, MC 847, Chicago, IL 60612, USA.
Daniel LantvitDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St, suite 130 CSN, MC 847, Chicago, IL 60612, USA.
Hui ChenMass Spectrometry Core, University of Illinois at Chicago, 835 S. Wolcott Ave., suite E12, Chicago, IL 60612, USA.
Sunil HwangMass Spectrometry Core, University of Illinois at Chicago, 835 S. Wolcott Ave., suite E12, Chicago, IL 60612, USA.
Natalia NietoDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St, suite 130 CSN, MC 847, Chicago, IL 60612, USA; Department of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, 840 S. Wood St., suite 1020N, MC 787, Chicago, IL 60612, USA; Research & Development Service, Jesse Brown Veterans Affairs Medical Center, Chicago, IL, USA. Electronic address: nnieto@uic.edu.
University of Illinois Chicago · USJesse Brown VA Medical Center · US

Funding

Protective role of OPN-High macrophages in NASHR01DK134461 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Natalia Nieto · 2023 to 2026
$2.1M
Pathogenic role of hepatocyte-derived high-mobility group box-1 isoforms as potential therapeutic targets to prevent and/or resolve liver fibrosisR01DK111677 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NIETO, NATALIA · 2017 to 2020
$2.0M
High-mobility group box-1 and alcoholic liver diseaseR01AA025907 · NIAAA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NIETO, NATALIA · 2018 to 2022
$1.8M
Acquisition of a Q-Exactive HF Mass SpectrometerS10OD027016 · OD · UNIVERSITY OF ILLINOIS AT CHICAGO · PI COLOGNA, STEPHANIE M · 2019 to 2019
$600k
Pathogenic role of a protein complex of liver origin as regulator of a proinflammatory program that drives hepatic and intestinal injury in alcoholic liver diseaseI01BX005093 · VA · JESSE BROWN VA MEDICAL CENTER · PI NIETO, NATALIA · 2021 to 2025
–
BLRD VA I01 BX005093NIAAA NIH HHS R01 AA025907NIDDK NIH HHS R01 DK111677NIDDK NIH HHS R01 DK134461NIH HHS S10 OD027016
6 · The paper itself

Abstract

BACKGROUND &

aimsHigh-mobility group box-1 (HMGB1) significantly increases and undergoes post-translational modifications (PTMs) in response to liver injury. Since oxidative stress plays a major role in liver fibrosis and induces PTMs in proteins, we hypothesized that redox-sensitive HMGB1 isoforms contribute to liver fibrosis progression and resolution.

methodsWe used ESI-LC-MS (electrospray ionization-liquid chromatography-mass spectrometry) to study PTMs of HMGB1 during fibrosis progression and resolution. Conditional knockout mice were used for functional analyses.

resultsWe identified that disulfide ([O]) and sulfonated ([SO

conclusionDynamic changes in hepatocyte-derived [O] and [SO IMPACT AND IMPLICATIONS: Since oxidative stress plays a major role in liver fibrosis and induces post-translational modifications of proteins, we hypothesized that redox-sensitive HMGB1 isoforms contribute to liver fibrosis progression and resolution. This study is significant because a rise in [H] HMGB1 could flag 'patient at risk', the presence of [O] HMGB1 could suggest 'disease in progress or active scarring', while the appearance of [SO

Indexed as

Carbon TetrachlorideHMGB1 ProteinAnimalsCells, CulturedHumansLiver CirrhosisMiceMice, KnockoutOxidation-ReductionProtein IsoformsReceptor for Advanced Glycation End ProductsCarbon TetrachlorideHMGB1 ProteinHMGB1 protein, mouseProtein IsoformsReceptor for Advanced Glycation End Productsapoptosiscollagenhepatic stellate cellshepatocytespost-translational modificationsreceptor for advanced-glycosylation end-products

Identifiers

PMID37989401
PMCPMC10923114
OpenAlexW4388806532

What OpenQuestion holds

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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.