Evidence map›Paper›PMID 32295146›Full record

SynthesisInternational journal of molecular sciences2020

Targeting High Mobility Group Box 1 in Subarachnoid Hemorrhage: A Systematic Review.

Sajjad Muhammad, Shafqat Rasul Chaudhry, Ulf Dietrich Kahlert, Martin Lehecka, Miikka Korja, Mika Niemelä, Daniel Hänggi

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 3 pooled it
1.3field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 3 syntheses or guidelines pooled it, 25 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

7 authors at 3 institutions in 3 countries.

Sajjad MuhammadDepartment of Neurosurgery, Heinrich-Heine University Medical Center, 40225 Düsseldorf, Germany.ORCID 0000-0002-6734-7979
Shafqat Rasul ChaudhryShifa College of Pharmaceutical Sciences, Shifa Tameer-e-Millat University, Islamabad 44000, Pakistan.
Ulf Dietrich KahlertDepartment of Neurosurgery, Heinrich-Heine University Medical Center, 40225 Düsseldorf, Germany.
Martin LeheckaDepartment of Neurosurgery, University of Helsinki and Helsinki University Hospital, 00014 Helsinki, Finland.
Miikka KorjaDepartment of Neurosurgery, University of Helsinki and Helsinki University Hospital, 00014 Helsinki, Finland.
Mika NiemeläDepartment of Neurosurgery, University of Helsinki and Helsinki University Hospital, 00014 Helsinki, Finland.
Daniel HänggiDepartment of Neurosurgery, Heinrich-Heine University Medical Center, 40225 Düsseldorf, Germany.
University of Helsinki · FIDüsseldorf University Hospital · DEShifa Tameer-e-Millat University · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aneurysmal subarachnoid hemorrhage (aSAH) is a complex and potentially deadly disease. Neurosurgical clipping or endovascular coiling can successfully obliterate ruptured aneurysms in almost every case. However, despite successful interventions, the clinical outcomes of aSAH patients are often poor. The reasons for poor outcomes are numerous, including cerebral vasospasm (CVS), post-hemorrhagic hydrocephalus, systemic infections and delayed cerebral ischemia. Although CVS with subsequent cerebral ischemia is one of the main contributors to brain damage after aSAH, little is known about the underlying molecular mechanisms of brain damage. This review emphasizes the importance of pharmacological interventions targeting high mobility group box 1 (HMGB1)-mediated brain damage after subarachnoid hemorrhage (SAH) and CVS. We searched Pubmed, Ovid medline and Scopus for "subarachnoid hemorrhage" in combination with "HMGB1". Based on these criteria, a total of 31 articles were retrieved. After excluding duplicates and selecting the relevant references from the retrieved articles, eight publications were selected for the review of the pharmacological interventions targeting HMGB1 in SAH. Damaged central nervous system cells release damage-associated molecular pattern molecules (DAMPs) that are important for initiating, driving and sustaining the inflammatory response following an aSAH. The discussed evidence suggested that HMGB1, an important DAMP, contributes to brain damage during early brain injury and also to the development of CVS during the late phase. Different pharmacological interventions employing natural compounds with HMGB1-antagonizing activity, antibody targeting of HMGB1 or scavenging HMGB1 by soluble receptors for advanced glycation end products (sRAGE), have been shown to dampen the inflammation mediated brain damage and protect against CVS. The experimental data suggest that HMGB1 inhibition is a promising strategy to reduce aSAH-related brain damage and CVS. Clinical studies are needed to validate these findings that may lead to the development of potential treatment options that are much needed in aSAH.

Indexed as

AnimalsAntibodies, MonoclonalBiomarkersDisease ManagementDisease SusceptibilityHMGB1 ProteinHumansMolecular Targeted TherapySubarachnoid HemorrhageVasospasm, IntracranialAntibodies, MonoclonalBiomarkersHMGB1 ProteinalarminsCVS (Cerebral vasospasm)damage-associated molecular pattern molecules (DAMPs)HMGB1 (High mobility group box 1)subarachnoid hemorrhage

Identifiers

PMID32295146
PMCPMC7215307
OpenAlexW3016485579

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.