Evidence map›Paper›PMID 7515561›Full record

ArticleThe American journal of pathology1994

Time course of complement activation and inhibitor expression after ischemic injury of rat myocardium.

A Väkevä, B P Morgan, I Tikkanen, K Helin, P Laurila, S Meri

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PubMed Full text at PMC
In one paragraph

Article in The American journal of pathology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Inflammation in myocardial injury: mesenchymal stem cells as potential immunomodulators.American journal of physiology. Heart and circulatory physiology · 2019
    Review
  12. Article
  13. Review
  14. Article
  15. Observational
  16. Article
  17. Early markers for myocardial ischemia and sudden cardiac death.International journal of legal medicine · 2016
    Article
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

A VäkeväDepartment of Bacteriology and Immunology, University of Helsinki, Finland.
B P Morgan
I Tikkanen
K Helin
P Laurila
S Meri
University of Helsinki · FI

Funding

Wellcome Trust
6 · The paper itself

Abstract

Activation of the complement (C) system has been documented in both experimental and clinical studies of myocardial infarction, but the exact time course and mechanisms leading to C activation have remained unclear. Our earlier postmortem study on human beings showed that formation of the membrane attack complex (MAC) of C was associated with loss of CD59 (protectin), an important sarcolemmal regulator of MAC, from the infarcted area. The recent discovery of a rat analogue of CD59 has now allowed the first experimental evaluation of the temporal and spatial relationship between C component deposition and loss of CD59 in acute myocardial infarction (AMI). After ligating the left coronary artery in rats the earliest sign of C activation, focal deposition of C3, was observed at 2 hours. Deposition of the early (C1, C3) and late pathway (C8, C9) components in the AMI lesions occurred at 3 hours. Glycophosphoinositol-anchored rat CD59 was expressed in the sarcolemmal membranes of normal cardiomyocytes. In Western blot analysis extracts of normal rat heart CD59 appeared as a band of 21 kd of molecular weight under nonreducing conditions. Loss of CD59 in the AMI lesions was observed in association with deposits of MAC from day one onward. Our results show that C activation universally accompanies AMI in vivo. It is initiated within 2 hours after coronary artery obstruction via deposition of C3, which may be due to generation of the alternative pathway C3 convertase in the ischemic area. Deposition of C1 and late C components also starts during the early hours (2 to 4 hours) after ischemia. Subsequent loss of the protective CD59 antigen may initiate postinjury clearance of the irreversibly damaged tissue.

Indexed as

AnimalsAntigens, CDBlotting, WesternCD59 AntigensComplement ActivationComplement C1Complement C3Complement C8Complement C9Complement Inactivator ProteinsComplement Membrane Attack ComplexDisease Models, AnimalElectrophoresis, Polyacrylamide GelImmunohistochemistryMaleMembrane GlycoproteinsAntigens, CDCD59 AntigensComplement C1Complement C3Complement C8Complement C9Complement Inactivator ProteinsComplement Membrane Attack ComplexMembrane GlycoproteinsType C Phospholipases

Identifiers

PMID7515561
PMCPMC1887457
OpenAlexW1536005089

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.