Evidence map›Paper›PMID 25652948›Full record

ReviewJournal of cardiovascular translational research2015

Cardiac allograft vasculopathy: a donor or recipient induced pathology?

Patricia van den Hoogen, Manon M H Huibers, Joost P G Sluijter, Roel A de Weger

Abstract readReview
In one paragraph

Review in Journal of cardiovascular translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Comprehensive Analysis of Cardiac Xeno-Graft Unveils Rejection Mechanisms.International journal of molecular sciences · 2021
    Article
  7. Review
  8. Transplantation of Hearts Donated after Circulatory Death.Frontiers in cardiovascular medicine · 2018
    Review
  9. Cardiac allograft vasculopathy in Dutch heart transplant recipients.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2016
    Article
  10. Article
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

4 authors.

Patricia van den HoogenDepartment of Cardiology, Experimental Cardiology laboratory, University Medical Centre Utrecht, Utrecht, The Netherlands.
Manon M H Huibers
Joost P G Sluijter
Roel A de Weger

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac allograft vasculopathy (CAV) is one of the main causes of late-stage heart failure after heart transplantation. CAV is characterized by concentric luminal narrowing of the coronary arteries, but the exact pathogenesis of CAV is still not unraveled. Many researchers show evidence of an allogeneic immune response of the recipient, whereas others show contrasting results in which donor-derived cells induce an immune response against the graft. In addition, fibrosis of the neo-intima can be induced by recipient-derived circulating cells or donor-derived cells. In this review, both donor and recipient sides of the story are described to obtain better insight in the pathogenesis of CAV. Dual outcomes were found regarding the contribution of donor and recipient cells in the initiation of the immune response and the development of fibrosis during CAV. Future research could focus more on the potential synergistic interaction of donor and recipient cells leading to CAV.

Indexed as

Tissue DonorsTransplant RecipientsAllograftsAnimalsCoronary Artery DiseaseCoronary VesselsFibrosisGraft RejectionHeart FailureHeart TransplantationHumansNeointimaRisk FactorsTreatment Outcome

Identifiers

PMID25652948
PMCPMC4382530

What OpenQuestion holds

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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.