Evidence map›Paper›PMID 14507653›Full record

ArticleThe American journal of pathology2003

Nontransgenic hyperexpression of a complement regulator in donor kidney modulates transplant ischemia/reperfusion damage, acute rejection, and chronic nephropathy.

Julian R Pratt, Miriam E Jones, Jun Dong, Wuding Zhou, Paramit Chowdhury, Richard A G Smith, Steven H Sacks

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 88 citations in OpenAlex.

  1. Trial
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  10. Increasing the efficacy and safety of a human complement inhibitor for treating post-transplant cardiac ischemia reperfusion injury by targeting to a graft-specific neoepitope.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2021
    Article
  11. Frontiers in immunology · 2021
    Article
  12. Review
  13. Review
  14. Article
  15. What Is Direct Allorecognition?Current transplantation reports · 2016
    Review
  16. The Complement System and Antibody-Mediated Transplant Rejection.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Review
  17. Review
  18. Article
  19. Review
  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

7 authors at 4 institutions in 3 countries.

Julian R PrattDepartment of Renal Medicine and Transplantation, King's College, University of London, London, United Kingdom.
Miriam E Jones
Jun Dong
Wuding Zhou
Paramit Chowdhury
Richard A G Smith
Steven H Sacks
King's College London · GBOntotext (Bulgaria) · BGUniversidad de Londres · MXUniversity of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement activation during ischemia and reperfusion contributes to the development of tissue injury with severe negative impact on outcomes in transplantation. To counter the effect of complement, we present a strategy to deliver a novel complement regulator stabilized on cell surfaces within donor organs. The membrane-bound complement regulator is able to inhibit complement activation when the donor organ is revascularized and exposed to host-circulating complement. Application of this construct to donor kidneys protected transplanted tissues from ischemia/reperfusion injury and reduced the deposition of activated complement and histological signs of damage under conditions in which a nontargeted control construct was ineffective. Treatment of donor organs in this way improved graft performance in the short and long term. An analysis of the immune response in allograft recipients showed that reducing graft damage at the time of transplantation through complement regulation also modulated the alloresponse. Additionally, the results of perfusion studies with human kidneys demonstrated the feasibility of targeting endothelial and epithelial surfaces with this construct, to allow investigation in clinical transplantation.

Indexed as

Kidney TransplantationRenal CirculationAcute DiseaseAnimalsChronic DiseaseEndotheliumEpithelial CellsGraft RejectionHumansIn Vitro TechniquesKidneyKidney DiseasesPeptide FragmentsRatsRats, Inbred F344Rats, Inbred Lewm-pSCR1-3 protein, humanPeptide FragmentsReceptors, Cell SurfaceReceptors, Complement 3b

Identifiers

PMID14507653
PMCPMC3278791
OpenAlexW2013804060

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.