Evidence map›Paper›PMID 34191093›Full record

ReviewSeminars in immunopathology2021

Complement as driver of systemic inflammation and organ failure in trauma, burn, and sepsis.

Marco Mannes, Christoph Q Schmidt, Bo Nilsson, Kristina N Ekdahl, Markus Huber-Lang

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Diffuse alveolar damage, acute respiratory distress syndrome (ARDS), and non-cardiogenic pulmonary edema. Part 1: ARDS endotypes, including systemic inflammatory response syndrome and sepsis, with dog and cat examples.Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2026
    Review
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  7. Article
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  11. Article
  12. Article
  13. Article
  14. Thromboinflammatory complications ofFrontiers in immunology · 2025
    Review
  15. Review
  16. Immune Landscape in Kidney Transplantation.Journal of inflammation research · 2025
    Review
  17. Article
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  19. Review
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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

5 authors at 3 institutions in 2 countries.

Marco MannesInstitute of Clinical and Experimental Trauma-Immunology, University Hospital of Ulm, Helmholtzstr. 8/2, 89081, Ulm, Germany.
Christoph Q SchmidtInstitute of Pharmacology of Natural Products and Clinical Pharmacology, Ulm University, Ulm, Germany.
Bo NilssonDepartment of Immunology, Genetics and Pathology (IGP), Rudbeck Laboratory C5:3, Uppsala University, Uppsala, Sweden.
Kristina N EkdahlDepartment of Immunology, Genetics and Pathology (IGP), Rudbeck Laboratory C5:3, Uppsala University, Uppsala, Sweden.
Markus Huber-LangInstitute of Clinical and Experimental Trauma-Immunology, University Hospital of Ulm, Helmholtzstr. 8/2, 89081, Ulm, Germany. markus.huber-lang@uniklinik-ulm.de.ORCID 0000-0003-2359-6516
Uppsala University · SEUniversität Ulm · DEUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement is one of the most ancient defense systems. It gets strongly activated immediately after acute injuries like trauma, burn, or sepsis and helps to initiate regeneration. However, uncontrolled complement activation contributes to disease progression instead of supporting healing. Such effects are perceptible not only at the site of injury but also systemically, leading to systemic activation of other intravascular cascade systems eventually causing dysfunction of several vital organs. Understanding the complement pathomechanism and its interplay with other systems is a strict requirement for exploring novel therapeutic intervention routes. Ex vivo models exploring the cross-talk with other systems are rather limited, which complicates the determination of the exact pathophysiological roles that complement has in trauma, burn, and sepsis. Literature reporting on these three conditions is often controversial regarding the importance, distribution, and temporal occurrence of complement activation products further hampering the deduction of defined pathophysiological pathways driven by complement. Nevertheless, many in vitro experiments and animal models have shown beneficial effects of complement inhibition at different levels of the cascade. In the future, not only inhibition but also a complement reconstitution therapy should be considered in prospective studies to expedite how meaningful complement-targeted interventions need to be tailored to prevent complement augmented multi-organ failure after trauma, burn, and sepsis.This review summarizes clinically relevant studies investigating the role of complement in the acute diseases trauma, burn, and sepsis with important implications for clinical translation.

Indexed as

BurnsSepsisAnimalsComplement System ProteinsHumansInflammationProspective StudiesComplement System ProteinsBurnClinical translationComplement activationSepsisSystemic inflammationThromboinflammationTrauma

Identifiers

PMID34191093
PMCPMC8243057
OpenAlexW3174418245

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.