Evidence map›Paper›PMID 37048161›Full record

ReviewCells2023

High Mobility Group Box 1 (HMGB1): Potential Target in Sepsis-Associated Encephalopathy.

Bram DeWulf, Laurens Minsart, Franck Verdonk, Véronique Kruys, Michael Piagnerelli, Mervyn Maze, Sarah Saxena

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.1field-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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Serum HMGB1 and Alcohol-Related Liver Disease.Journal of clinical medicine · 2026
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  8. p65 enhanced METTL3-mediated mCentral-European journal of immunology · 2025
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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

7 authors at 5 institutions in 3 countries.

Bram DeWulfDepartment of Anesthesia-Critical Care, AZ Sint-Jan Brugge Oostende AV, 8000 Bruges, Belgium.
Laurens MinsartDepartment of Anesthesia, Antwerp University Hospital (UZA), 2650 Edegem, Belgium.
Franck VerdonkDepartment of Anesthesiology and Intensive Care, GRC 29, DMU DREAM, Hôpital Saint-Antoine and Sorbonne University, Assistance Publique-Hôpitaux de Paris, 75012 Paris, France.
Véronique KruysLaboratory of Molecular Biology of the Gene, Department of Molecular Biology, Free University of Brussels (ULB), 6041 Gosselies, Belgium.
Michael PiagnerelliDepartment of Intensive Care, CHU-Charleroi, Université Libre de Bruxelles, 6042 Charleroi, Belgium.ORCID 0000-0002-9201-827X
Mervyn MazeCenter for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California San Francisco, San Francisco, CA 94143, USA.ORCID 0000-0001-9794-2472
Sarah SaxenaDepartment of Anesthesia-Critical Care, AZ Sint-Jan Brugge Oostende AV, 8000 Bruges, Belgium.
AZ Sint-Jan · BEAntwerp University Hospital · BESorbonne Université · FRUniversité Libre de Bruxelles · BEUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis-associated encephalopathy (SAE) remains a challenge for intensivists that is exacerbated by lack of an effective diagnostic tool and an unambiguous definition to properly identify SAE patients. Risk factors for SAE development include age, genetic factors as well as pre-existing neuropsychiatric conditions. Sepsis due to certain infection sites/origins might be more prone to encephalopathy development than other cases. Currently, ICU management of SAE is mainly based on non-pharmacological support. Pre-clinical studies have described the role of the alarmin high mobility group box 1 (HMGB1) in the complex pathogenesis of SAE. Although there are limited data available about the role of HMGB1 in neuroinflammation following sepsis, it has been implicated in other neurologic disorders, where its translocation from the nucleus to the extracellular space has been found to trigger neuroinflammatory reactions and disrupt the blood-brain barrier. Negating the inflammatory cascade, by targeting HMGB1, may be a strategy to complement non-pharmacologic interventions directed against encephalopathy. This review describes inflammatory cascades implicating HMGB1 and strategies for its use to mitigate sepsis-induced encephalopathy.

Indexed as

Brain DiseasesHMGB1 ProteinSepsisSepsis-Associated EncephalopathyAlarminsHumansAlarminsHMGB1 Proteinhigh mobility group box 1HMGB1sepsissepsis-associated encephalopathy

Identifiers

PMID37048161
PMCPMC10093266
OpenAlexW4362619951

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.