Evidence map›Paper›PMID 22705194›Full record

ArticleCardiovascular pathology : the official journal of the Society for Cardiovascular Pathology

The effect of C1 inhibitor on myocardial ischemia and reperfusion injury.

Fengxin Lu, Stacey M Fernandes, Alvin E Davis

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Therapeutic Potential of C1-Inhibitor in Vascular Diseases and Beyond.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Intrauterine Programming of Diabetes Induced Cardiac Embryopathy.Diabetes & obesity international journal · 2019
    Article
  10. Article
  11. Review
  12. Complement Dependence of Murine Costimulatory Blockade-Resistant Cellular Cardiac Allograft Rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Observational
  17. Review
  18. Review
  19. Treatment with anti-C5a antibody improves the outcome of H7N9 virus infection in African green monkeys.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2015
    Article
  20. Mannan-binding lectin in cardiovascular disease.BioMed research international · 2014
    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 1 institution in 1 country.

Fengxin LuImmune Disease Institute, Harvard Medical School, 3 Blackfan Circle, Boston, MA 02115, USA. fengxinlu@gmail.com
Stacey M Fernandes
Alvin E Davis
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

backgroundActivation of the complement system has been demonstrated to be an important mechanism in the mediation of myocardial ischemia and reperfusion (MIR) injury. C1 inhibitor (C1INH) has been shown to be beneficial in experimental MIR models. The underlying mechanism of this effect has been assumed to result primarily from inhibition of complement system activation. We recently demonstrated that C1INH plays a direct role in suppression of leukocyte transmigration in the mouse intestinal ischemia and reperfusion model. The purpose of this study was to investigate the mechanism of the beneficial effect of C1INH in mouse MIR model.

methodsC57BL/6, C1INH-deficient (C1INH(-/-)), and C3-deficient mice (C3(-/-)) were subjected to 30-min (C57BL/6 and C1INH(-/-)) or 60-min (C3(-/-)) occlusion of the left anterior descending branch of the coronary artery followed by 4-h reperfusion. C1INH or reactive center cleaved inactive C1INH (iC1INH) was injected intravenously 5 min before reperfusion.

resultsMyocardial infarct size relative to the area at risk or relative to left ventricular area was significantly reduced in C1INH-treated wild-type, C1INH(-/-), and C3(-/-) mice compared with vehicle-treated mice. MIR induced an increase in myocardial polymorphonuclear neutrophil accumulation and plasma cardiac specific troponin I levels in vehicle-treated MIR mice, while C1INH treatment significantly attenuated these effects. iC1INH had a similar protective effect.

conclusionsThese results suggested that C1INH prevented MIR injury in mice and that this cardioprotective effect may not solely result from complement inhibition, but might be also contributed by inhibiting leukocyte recruitment into ischemic tissue, an effect that is not mediated via protease inhibition.

Indexed as

AnimalsBiomarkersChemotaxis, LeukocyteComplement ActivationComplement C1 Inhibitor ProteinComplement C3Disease Models, AnimalInjections, IntravenousMaleMiceMice, Inbred C57BLMice, KnockoutMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumNeutrophil InfiltrationBiomarkersComplement C1 Inhibitor ProteinComplement C3Serping1 protein, mouseTroponin I

Identifiers

PMID22705194
PMCPMC3449044
OpenAlexW2137169303

What Socratic 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 Socratic graph.