Evidence map›Paper›PMID 18674818›Full record

ReviewMolecular immunology2008

Biological activities of C1 inhibitor.

Alvin E Davis, Pedro Mejia, Fengxin Lu

Open access · greenAbstract readReview
In one paragraph

Review in Molecular immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

149 citing papers in PubMed, 1 synthesis or guideline pooled it, 298 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Garadacimab for the long-term prophylaxis of hereditary angioedema.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2026
    Review
  8. Article
  9. Review
  10. Complement system in cancer: friend or foe of immunotherapy.Journal for immunotherapy of cancer · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Targeting C1q signaling in fibro-adipogenic progenitors prevents regenerative fibrosis of aged muscle.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  15. Review
  16. Article
  17. Article
  18. Defining the Features of Complement-Active IgM.Journal of molecular biology · 2025
    Article
  19. Article
  20. Review

89 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

3 authors at 1 institution in 1 country.

Alvin E DavisHarvard Medical School, Immune Disease Institute, Boston, MA 02115, USA. aldavis@idi.harvard.edu
Pedro Mejia
Fengxin Lu
Harvard University · US

Funding

C1 INHIBITOR GENE AND HEREDITARY ANGIONEUROTIC EDEMAR37HD022082 · NICHD · IMMUNE DISEASE INSTITUTE, INC. · PI DAVIS, ALVIN E · 1999 to 2008
$3.9M
C1 INHIBITOR-MEDIATED PROTECTION FROM ENDOTOXIN SHOCKR01AI057366 · NIAID · IMMUNE DISEASE INSTITUTE, INC. · PI DAVIS, ALVIN E · 2005 to 2009
$2.3M
NIAID NIH HHS R01 AI057366NIAID NIH HHS R01-AI057366NICHD NIH HHS R37 HD022082NICHD NIH HHS R37-HD22082
6 · The paper itself

Abstract

Broadly speaking, C1 inhibitor plays important roles in the regulation of vascular permeability and in the suppression of inflammation. Vascular permeability control is exerted largely through inhibition of two of the proteases involved in the generation of bradykinin, factor XIIa and plasma kallikrein (the plasma kallikrein-kinin system). Anti-inflammatory functions, however, are exerted via several activities including inhibition of complement system proteases (C1r, C1s, MASP2) and the plasma kallikrein-kinin system proteases, in addition to interactions with a number of different proteins, cells and infectious agents. These more recently described, as yet incompletely characterized, activities serve several potential functions, including concentration of C1 inhibitor at sites of inflammation, inhibition of alternative complement pathway activation, inhibition of the biologic activities of gram negative endotoxin, enhancement of bacterial phagocytosis and killing, and suppression of the influx of leukocytes into a site of inflammation. C1 inhibitor has been shown to be therapeutically useful in a variety of animal models of inflammatory diseases, including gram negative bacterial sepsis and endotoxin shock, suppression of hyperacute transplant rejection, and treatment of a variety of ischemia-reperfusion injuries (heart, intestine, skeletal muscle, liver, brain). In humans, early data appear particularly promising in myocardial reperfusion injury. The mechanism (or mechanisms) of the effect of C1 inhibitor in these conditions is (are) not completely clear, but involve inhibition of complement and contact system activation, in addition to variable contributions from other C1 inhibitor activities that do not involve protease inhibition.

Indexed as

AnimalsComplement C1Complement C1 Inactivator ProteinsComplement C1 Inhibitor ProteinEndopeptidasesFactor XIIaHumansKallikreinsPeptide HydrolasesProtein BindingReperfusion InjurySerpinsShock, SepticComplement C1Complement C1 Inactivator ProteinsComplement C1 Inhibitor ProteinEndopeptidasesFactor XIIaKallikreinsPeptide HydrolasesSerpins

Identifiers

PMID18674818
PMCPMC2626406
OpenAlexW1996868603

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.