Evidence map›Paper›PMID 32426849›Full record

ArticleHepatology (Baltimore, Md.)2021

Disulfide High-Mobility Group Box 1 Drives Ischemia-Reperfusion Injury in Human Liver Transplantation.

Rebecca A Sosa, Allyson Q Terry, Fady M Kaldas, Yi-Ping Jin, Maura Rossetti, Takahiro Ito, Fang Li, Richard S Ahn, Bita V Naini, Victoria M Groysberg and 8 more

Open access · greenAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 72 citations in OpenAlex.

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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

18 authors at 2 institutions in 1 country.

Rebecca A SosaDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.ORCID 0000-0002-9860-6830
Allyson Q TerryDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.ORCID 0000-0002-4156-991
Fady M KaldasDumont-UCLA Transplantation CenterDepartment of SurgeryDavid Geffen School of Medicine at UCLALos AngelesCA.
Yi-Ping JinDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.
Maura RossettiDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.ORCID 0000-0003-3347-6200
Takahiro ItoDumont-UCLA Transplantation CenterDepartment of SurgeryDavid Geffen School of Medicine at UCLALos AngelesCA.
Fang LiDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.
Richard S AhnInstitute of Quantitative and Computational BiosciencesDavid Geffen School of Medicine at UCLALos AngelesCA.ORCID 0000-0002-9698-2752
Bita V NainiDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.
Victoria M GroysbergDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.
Ying ZhengDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.
Antony AzizDumont-UCLA Transplantation CenterDepartment of SurgeryDavid Geffen School of Medicine at UCLALos AngelesCA.
Jessica Nevarez-MejiaDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.ORCID 0000-0003-3390-4818
Ali ZarrinparDumont-UCLA Transplantation CenterDepartment of SurgeryDavid Geffen School of Medicine at UCLALos AngelesCA.
Ronald W BusuttilDumont-UCLA Transplantation CenterDepartment of SurgeryDavid Geffen School of Medicine at UCLALos AngelesCA.ORCID 0000-0001-8157-1531
David W GjertsonDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.
Jerzy W Kupiec-WeglinskiDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.
Elaine F ReedDepartment of Pathology and Laboratory MedicineDavid Geffen School of Medicine at UCLALos AngelesCA.ORCID 0000-0002-3524-545
University of California, Los Angeles · USQuantitative BioSciences · US

Funding

UCLA Clinical Translational Science InstituteUL1TR001881 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARLEEN F. BROWN, ARASH NAEIM · 2016 to 2026
$118.1M
Regulation of Innate Immune Responses by Alloimmunity in Liver Ischemia-Reperfusion InjuryP01AI120944 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Jerzy W Kupiec-Weglinski · 2017 to 2026
$20.0M
UCLA Tumor Immunology Training ProgramT32CA009120 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Steven M. Dubinett, MICHAEL A TEITELL · 1985 to 2026
$10.3M
Vascular Biology Training GrantT32HL069766 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2002 to 2022
$7.4M
Systems Genetics Dissection of Non-alcoholic SteatohepatitisR01DK117850 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Aldons Jake Lusis · 2019 to 2026
$4.6M
Division of Cancer Prevention, National Cancer Institute T32CA009120National Center for Advancing Translational Sciences (NCATS) UL1TR001881National Institute of Allergy and Infectious Diseases P01AI120944NCATS NIH HHS UL1 TR001881NCI NIH HHS T32 CA009120NHLBI NIH HHS T32 HL069766NIAID NIH HHS P01 AI120944NIDDK NIH HHS R01 DK117850NIMHD NIH HHS L60 MD011903NIMHD NIH HHS L60MD011903
6 · The paper itself

Abstract

BACKGROUND AND

aimsSterile inflammation is a major clinical concern during ischemia-reperfusion injury (IRI) triggered by traumatic events, including stroke, myocardial infarction, and solid organ transplantation. Despite high-mobility group box 1 (HMGB1) clearly being involved in sterile inflammation, its role is controversial because of a paucity of patient-focused research. APPROACH AND

resultsHere, we examined the role of HMGB1 oxidation states in human IRI following liver transplantation. Portal blood immediately following allograft reperfusion (liver flush; LF) had increased total HMGB1, but only LF from patients with histopathological IRI had increased disulfide-HMGB1 and induced Toll-like receptor 4-dependent tumor necrosis factor alpha production by macrophages. Disulfide HMGB1 levels increased concomitantly with IRI severity. IRI

conclusionsThese data identify disulfide-HMGB1 as a mechanistic biomarker of, and therapeutic target for, minimizing sterile inflammation during human liver IRI.

Indexed as

CytokinesDisulfidesFemaleFluorescent Antibody TechniqueHMGB1 ProteinHumansLiverLiver TransplantationMaleMicroscopy, ConfocalMiddle AgedMonocytesReperfusion InjuryTissue DonorsCytokinesDisulfidesHMGB1 ProteinHMGB1 protein, human

Identifiers

PMID32426849
PMCPMC8722704
OpenAlexW3026994380

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Registered trials

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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.