Evidence map›Paper›PMID 24903097›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2014

Interacting mechanisms in the pathogenesis of cardiac allograft vasculopathy.

Jordan S Pober, Dan Jane-wit, Lingfeng Qin, George Tellides

Open access · greenAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

54 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Suppression of cardiac allograft vasculopathy by a macrophage efferocytosis receptor.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026
    Article
  6. Review
  7. Article
  8. Review
  9. Observational
  10. Observational
  11. Article
  12. Immunomodulation by allograft endothelial cells.Frontiers in transplantation · 2025
    Review
  13. Article
  14. Observational
  15. Article
  16. Article
  17. Article
  18. Clonal hematopoiesis of indeterminate potential and outcomes after heart transplantation: A multicenter study.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2023
    Article
  19. Article
  20. 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 at 1 institution in 1 country.

Jordan S PoberFrom the Departments of Immunobiology (J.S.P.), Internal Medicine (D.J.-w.), and Surgery (L.Q. and G.T.), Yale University School of Medicine, New Haven, CT. jordan.pober@yale.edu.
Dan Jane-witFrom the Departments of Immunobiology (J.S.P.), Internal Medicine (D.J.-w.), and Surgery (L.Q. and G.T.), Yale University School of Medicine, New Haven, CT.
Lingfeng QinFrom the Departments of Immunobiology (J.S.P.), Internal Medicine (D.J.-w.), and Surgery (L.Q. and G.T.), Yale University School of Medicine, New Haven, CT.
George TellidesFrom the Departments of Immunobiology (J.S.P.), Internal Medicine (D.J.-w.), and Surgery (L.Q. and G.T.), Yale University School of Medicine, New Haven, CT.
Yale University · US

Funding

SOCS-1 and endothelial dysfunction in graft arteriosclerosisP01HL070295 · NHLBI · YALE UNIVERSITY · PI POBER, JORDAN S · 2001 to 2010
$17.9M
IMMUNOHEMATOLOGY/TRANSFUSION MEDICINE RESEARCH TRAININGT32HL007974 · NHLBI · YALE UNIVERSITY · PI JEANNE E HENDRICKSON, Diane S Krause · 2001 to 2026
$8.1M
Regulating Anti-Endothelial T Cell Responses in Graft ArteriosclerosisR01HL109455 · NHLBI · YALE UNIVERSITY · PI BOTHWELL, ALFRED LM, POBER, JORDAN S · 2011 to 2014
$2.5M
Human and Translational ImmunologyT32AI089704 · NIAID · YALE UNIVERSITY · PI HEROLD, KEVAN C · 2010 to 2014
$994k
NHLBI NIH HHS P01 HL070295NHLBI NIH HHS R01 HL109455NHLBI NIH HHS R01-HL109455NHLBI NIH HHS T32 HL007974NIAID NIH HHS T32 AI089704NIAID NIH HHS T32-AI089704
6 · The paper itself

Abstract

Cardiac allograft vasculopathy is the major cause of late graft loss in heart transplant recipients. Histological studies of characteristic end-stage lesions reveal arterial changes consisting of a diffuse, confluent, and concentric intimal expansion containing graft-derived cells expressing smooth muscle markers, extracellular matrix, penetrating microvessels, and a host mononuclear cell infiltrate concentrated subjacent to an intact graft-derived luminal endothelial cell lining with little evidence of acute injury. This intimal expansion combined with inadequate compensatory outward remodeling produces severe generalized stenosis extending throughout the epicardial and intramyocardial arterial tree that causes ischemic graft failure. Cardiac allograft vasculopathy lesions affect ≥50% of transplant recipients and are both progressive and refractory to treatment, resulting in ≈5% graft loss per year through the first 10 years after transplant. Lesions typically stop at the suture line, implicating alloimmunity as the primary driver, but pathogenesis may be multifactorial. Here, we will discuss 6 potential contributors to lesion formation (1) conventional risk factors of atherosclerosis; (2) pre- or peritransplant injuries; (3) infection; (4) innate immunity; (5) T-cell-mediated immunity; and (6) B-cell-mediated immunity through production of donor-specific antibody. Finally, we will consider how these various mechanisms may interact with each other.

Indexed as

AllograftsAnimalsB-LymphocytesCommunicable DiseasesCoronary Artery DiseaseCoronary VesselsHeart TransplantationHumansImmunity, CellularImmunity, HumoralImmunity, InnateIsoantibodiesRisk FactorsSignal TransductionT-LymphocytesTreatment OutcomeIsoantibodiesT-lymphocytestransplantation

Identifiers

PMID24903097
PMCPMC4324618
OpenAlexW2155269095

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.