Evidence map›Paper›PMID 22129197›Full record

ReviewJournal of biomedical science2011

Molecular mechanisms of inflammation and tissue injury after major trauma--is complement the "bad guy"?

Miriam D Neher, Sebastian Weckbach, Michael A Flierl, Markus S Huber-Lang, Philip F Stahel

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of biomedical science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.4field-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

57 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
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  5. Article
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  8. Article
  9. Article
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  11. Review
  12. Review
  13. Intertwined pathways of complement activation command the pathogenesis of lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022
    Review
  14. [CRP apheresis in acute myocardial infarction and COVID-19].Medizinische Klinik, Intensivmedizin und Notfallmedizin · 2022
    Review
  15. Review
  16. Therapeutic Modulation of the Host Defense by Hemoadsorption with CytoSorbInternational journal of molecular sciences · 2021
    Article
  17. Soluble terminal complement activation fragment sC5b-9: a new serum biomarker for traumatic brain injury?European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2021
    Observational
  18. Article
  19. Review
  20. COVID-19 vasculitis and novel vasculitis mimics.The Lancet. Rheumatology · 2021
    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

5 authors at 2 institutions in 2 countries.

Miriam D NeherDepartment of Orthopaedic Surgery, University of Colorado Denver, School of Medicine, Denver Health Medical Center, 777 Bannock Street, Denver, CO 80204, USA.
Sebastian Weckbach
Michael A Flierl
Markus S Huber-Lang
Philip F Stahel
University of Colorado Denver · USUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trauma represents the leading cause of death among young people in industrialized countries. Recent clinical and experimental studies have brought increasing evidence for activation of the innate immune system in contributing to the pathogenesis of trauma-induced sequelae and adverse outcome. As the "first line of defense", the complement system represents a potent effector arm of innate immunity, and has been implicated in mediating the early posttraumatic inflammatory response. Despite its generic beneficial functions, including pathogen elimination and immediate response to danger signals, complement activation may exert detrimental effects after trauma, in terms of mounting an "innocent bystander" attack on host tissue. Posttraumatic ischemia/reperfusion injuries represent the classic entity of complement-mediated tissue damage, adding to the "antigenic load" by exacerbation of local and systemic inflammation and release of toxic mediators. These pathophysiological sequelae have been shown to sustain the systemic inflammatory response syndrome after major trauma, and can ultimately contribute to remote organ injury and death. Numerous experimental models have been designed in recent years with the aim of mimicking the inflammatory reaction after trauma and to allow the testing of new pharmacological approaches, including the emergent concept of site-targeted complement inhibition. The present review provides an overview on the current understanding of the cellular and molecular mechanisms of complement activation after major trauma, with an emphasis of emerging therapeutic concepts which may provide the rationale for a "bench-to-bedside" approach in the design of future pharmacological strategies.

Indexed as

AnimalsComplement ActivationComplement System ProteinsHumansImmunity, InnateInflammationWounds and InjuriesComplement System Proteins

Identifiers

PMID22129197
PMCPMC3247859
OpenAlexW2159154108

What OpenQuestion holds

Textmetadata
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.