Evidence map›Paper›PMID 32610502›Full record

ReviewInternational journal of molecular sciences2020

HMGB1-Mediated Neuroinflammatory Responses in Brain Injuries: Potential Mechanisms and Therapeutic Opportunities.

Yam Nath Paudel, Efthalia Angelopoulou, Christina Piperi, Iekhsan Othman, Mohd Farooq Shaikh

Open access · goldAbstract readReview
In one paragraph

Review 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 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
8.4field-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

68 citing papers in PubMed, 102 citations in OpenAlex.

  1. Trial
  2. Role of HMGB1 in Neuroinflammation.Molecular neurobiology · 2026
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8 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

5 authors at 2 institutions in 2 countries.

Yam Nath PaudelNeuropharmacology Research Strength, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor 47500, Malaysia.ORCID 0000-0002-8804-6331
Efthalia AngelopoulouDepartment of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Christina PiperiDepartment of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0000-0002-2701-0618
Iekhsan OthmanNeuropharmacology Research Strength, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor 47500, Malaysia.ORCID 0000-0001-9225-3678
Mohd Farooq ShaikhNeuropharmacology Research Strength, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor 47500, Malaysia.ORCID 0000-0001-9865-6224
Monash University Malaysia · MYNational and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain injuries are devastating conditions, representing a global cause of mortality and morbidity, with no effective treatment to date. Increased evidence supports the role of neuroinflammation in driving several forms of brain injuries. High mobility group box 1 (HMGB1) protein is a pro-inflammatory-like cytokine with an initiator role in neuroinflammation that has been implicated in Traumatic brain injury (TBI) as well as in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Herein, we discuss the implication of HMGB1-induced neuroinflammatory responses in these brain injuries, mediated through binding to the receptor for advanced glycation end products (RAGE), toll-like receptor4 (TLR4) and other inflammatory mediators. Moreover, we provide evidence on the biomarker potential of HMGB1 and the significance of its nucleocytoplasmic translocation during brain injuries along with the promising neuroprotective effects observed upon HMGB1 inhibition/neutralization in TBI and EBI induced by SAH. Overall, this review addresses the current advances on neuroinflammation driven by HMGB1 in brain injuries indicating a future treatment opportunity that may overcome current therapeutic gaps.

Indexed as

AnimalsBrain InjuriesBrain Injuries, TraumaticCytokinesHMGB1 ProteinHumansInflammationMicrogliaNeuroimmunomodulationNeuroprotective AgentsReceptor for Advanced Glycation End ProductsSignal TransductionSubarachnoid HemorrhageToll-Like Receptor 4CytokinesHMGB1 ProteinNeuroprotective AgentsReceptor for Advanced Glycation End ProductsToll-Like Receptor 4biomarkerhigh mobility group box 1 (HMGB1)neuroinflammationsubarachnoid hemorrhage (SAH)traumatic brain injury (TBI)

Identifiers

PMID32610502
PMCPMC7370155
OpenAlexW3037900192

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.