Evidence map›Paper›PMID 33290884›Full record

ReviewThrombosis research2021

Links between thrombosis and inflammation in traumatic brain injury.

W Brad Hubbard, Jing-Fei Dong, Miguel A Cruz, Rolando E Rumbaut

Open access · greenAbstract readReview
In one paragraph

Review in Thrombosis research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
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  9. Review
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  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Neurosteroid Receptor Modulators for Treating Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
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

4 authors at 4 institutions in 1 country.

W Brad HubbardLexington VA Healthcare System, Lexington, KY, United States of America; Spinal Cord and Brain Injury Research Center (SCoBIRC), University of Kentucky, Lexington, KY, United States of America. Electronic address: bradhubbard@uky.edu.
Jing-Fei DongBloodworks Research Institute, Seattle, WA, United States of America; Division of Hematology, Department of Medicine, University of Washington, Seattle, WA, United States of America.
Miguel A CruzCenter for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, TX, United States of America; Baylor College of Medicine, Houston, TX, United States of America.
Rolando E RumbautCenter for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, TX, United States of America; Baylor College of Medicine, Houston, TX, United States of America.
Baylor College of Medicine · USBloodworks Northwest · USMichael E. DeBakey VA Medical Center · USUniversity of Kentucky · US

Funding

von Willebrand Factor in Traumatic Brain Injury and Associated CoagulopathyR01HL152200 · NHLBI · BLOODWORKS · PI DONG, JING-FEI · 2020 to 2023
$3.1M
Traumatic Brain Injury-induced CoagulopathyR21NS087296 · NINDS · BLOODWORKS · PI DONG, JING-FEI · 2014 to 2015
$507k
Platelets and microvascular thrombosis in inflammationI01BX002551 · VA · MICHAEL E DEBAKEY VA MEDICAL CENTER · PI RUMBAUT, ROLANDO E · 2016 to 2025
–
Psychological deficits after low level blast exposure: role of neurovascular disruptionIK2BX004618 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI HUBBARD, WILLIAM BRAD · 2020 to 2024
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BLRD VA I01 BX002551BLRD VA IK2 BX004618NHLBI NIH HHS R01 HL152200NINDS NIH HHS R21 NS087296
6 · The paper itself

Abstract

Traumatic brain injury (TBI) continues to be a major healthcare problem and there is much to be explored regarding the secondary pathobiology to identify early predictive markers and new therapeutic targets. While documented changes in thrombosis and inflammation in major trauma have been well described, growing evidence suggests that isolated TBI also results in systemic alterations in these mechanisms. Here, we review recent experimental and clinical findings that demonstrate how blood-brain barrier dysfunction, systemic immune response, inflammation, platelet activation, and thrombosis contribute significantly to the pathogenesis of TBI. Despite advances in the links between thrombosis and inflammation, there is a lack of treatment options aimed at both processes and this could be crucial to treating vascular injury, local and systemic inflammation, and secondary ischemic events following TBI. With emerging evidence of newly-identified roles for platelets, leukocytes, the coagulation system and extracellular vesicles in processes of inflammation and thrombosis, there is a growing need to characterize these mechanisms within the context of TBI and whether these changes persist into the chronic phase of injury. Importantly, this review defines areas in need of further research to advance the field and presents a roadmap to identify new diagnostic and treatment options for TBI.

Indexed as

Brain Injuries, TraumaticThrombosisBlood PlateletsHumansInflammationPlatelet ActivationBiomarkersBlast injuryBlood-brain barrier dysfunctionCoagulopathyExtracellular vesiclesFibrinogenHemostasisMild TBIPlateletsvon Willebrand factor

Identifiers

PMID33290884
PMCPMC7867616
OpenAlexW3109353757

What OpenQuestion holds

Textmetadata
LicenceTDM
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.