Evidence map›Paper›PMID 26132735›Full record

ReviewCurrent opinion in organ transplantation2015

Effects of complement activation on allograft injury.

Joong Hyuk Sheen, Peter S Heeger

Abstract readReview
In one paragraph

Review in Current opinion in organ transplantation, 2015. 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
2.9field-weighted citation impact, top 8% 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, 34 citations in OpenAlex.

  1. The importance of B cells for osteogenic homeostasis.Cell communication and signaling : CCS · 2026
    Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Role of Complement Activation in Allograft Inflammation.Current transplantation reports · 2019
    Article
  9. Review
  10. Article
  11. Review
  12. Synthetic Biology in Cell and Organ Transplantation.Cold Spring Harbor perspectives in biology · 2017
    Review
  13. Article
  14. Complement in Kidney Transplantation.Frontiers in medicine · 2017
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. 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

2 authors at 1 institution in 1 country.

Joong Hyuk SheenDepartment of Medicine, Translational Transplant Research Center, Recanati Miller Transplant Institute and the Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, USA.
Peter S Heeger
Icahn School of Medicine at Mount Sinai · US

Funding

Complement & T Cell Medicated Allograft RejectionR01AI071185 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HEEGER, PETER SCOTT · 2007 to 2016
$4.3M
Complement & T Cell Medicated Allograft RejectionR56AI071185 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HEEGER, PETER SCOTT · 2012 to 2012
$339k
NIAID NIH HHS AI071185NIAID NIH HHS R01 AI071185NIAID NIH HHS R56 AI071185
6 · The paper itself

Abstract

purpose of reviewTo summarize the current knowledge regarding mechanisms linking the complement system to transplant injury, highlighting findings reported since 2013. RECENT

findingsBuilding upon the documentation that complement activation is a pathogenic mediator of posttransplant ischemia-reperfusion injury, emerging evidence from animal models indicates that blocking either the classical or lectin pathways attenuates ischemia-reperfusion injury. Immune cell-derived and locally activated complement, including intracellular C3, positively modulates alloreactive T-cell activation and expansion, whereby simultaneously inhibiting regulatory T-cell induction and function, and together promoting transplant rejection. Although alloantibody-initiated complement activation directly injures target cells, complement-dependent signals activate endothelial cells to facilitate T-cell-dependent inflammation. Complement activation within allografts contributes to progressive chronic injury and fibrosis. SUMMARY: The complement cascade, traditionally considered to be relevant to transplantation only as an effector mechanism of antibody-initiated allograft injury, is now understood to damage the allograft through multiple mechanisms. Complement activation promotes posttransplant ischemia-reperfusion injury, formation and function of alloantibody, differentiation and function of alloreactive T cells, and contributes to chronic progressive allograft failure. The recognition that complement affects transplant injury at many levels provides a foundation for targeting complement as a therapy to prolong transplant survival and improve patient health.

Indexed as

AllograftsComplement ActivationAnimalsComplement System ProteinsGraft RejectionGraft SurvivalHumansTransplantation, HomologousComplement System Proteins

Identifiers

PMID26132735
PMCPMC4510836
OpenAlexW2404755340

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.