Evidence map›Paper›PMID 22482043›Full record

ArticleCritical care research and practice2012

Manipulation of the complement system for benefit in sepsis.

Peter A Ward, Ren-Feng Guo, Niels C Riedemann

Open access · goldAbstract read
In one paragraph

Article in Critical care research and practice, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
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  5. Review
  6. Review
  7. Review
  8. Article
  9. Complement System: a Neglected Pathway in Immunotherapy.Clinical reviews in allergy & immunology · 2020
    Review
  10. Complement-induced activation of MAPKs and Akt during sepsis: role in cardiac dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  11. Inhibition of complement C5 protects against organ failure and reduces mortality in a baboon model ofProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  12. Complement-induced activation of the cardiac NLRP3 inflammasome in sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Protein kinase C-δ mediates sepsis-induced activation of complement 5a and urokinase-type plasminogen activator signaling in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014
    Article
  18. A novel C5a-neutralizing mirror-image (l-)aptamer prevents organ failure and improves survival in experimental sepsis.Molecular therapy : the journal of the American Society of Gene Therapy · 2013
    Article
  19. The role of complement system in septic shock.Clinical & developmental immunology · 2012
    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

3 authors at 2 institutions in 2 countries.

Peter A WardDepartment of Pathology, University of Michigan Medical School, 1301 Catherine Road, P.O. Box 5602, Ann Arbor, MI 48109-5602, USA.
Ren-Feng Guo
Niels C Riedemann
University of Michigan–Ann Arbor · USJena University Hospital · DE

Funding

Regulation of Lung Inflammation by Catecholamines and Adrenergic ReceptorsR01GM029507 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WARD, PETER A · 1985 to 2013
$3.9M
Protective Effects of Anti-C5a in SepsisR01GM061656 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WARD, PETER A · 2002 to 2013
$3.8M
LUNG INJURY BY OXYGEN METABOLITESR37GM029507 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WARD, PETER A · 1987 to 1996
–
NIGMS NIH HHS R01 GM029507NIGMS NIH HHS R01 GM061656NIGMS NIH HHS R37 GM029507
6 · The paper itself

Abstract

There is evidence in sepsis, both in rodents and in humans, that activation of the complement system results in excessive production of C5a, which triggers a series of events leading to septic shock, multiorgan failure, and lethality. In rodents following cecal ligation and puncture (CLP), which induces polymicrobial sepsis, in vivo blockade of C5a using neutralizing antibodies dramatically improved survival, reduced apoptosis of lymphoid cells, and attenuated the ensuing coagulopathy. Based on these data, it seems reasonable to consider therapeutic blockade of C5a in humans entering into sepsis and septic shock. Strategies for the development of such an antibody for use in humans are presented.

Identifiers

PMID22482043
PMCPMC3303540
OpenAlexW2089074620

What OpenQuestion holds

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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.