Evidence map›Paper›PMID 11390423›Full record

ArticleThe Journal of clinical investigation2001

Origin of neointimal endothelium and alpha-actin-positive smooth muscle cells in transplant arteriosclerosis.

J L Hillebrands, F A Klatter, B M van den Hurk, E R Popa, P Nieuwenhuis, J Rozing

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
27.5field-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

50 citing papers in PubMed, 287 citations in OpenAlex.

  1. Review
  2. Article
  3. CD34Theranostics · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Failing Heart Transplants and Rejection-A Cellular Perspective.Journal of cardiovascular development and disease · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Characteristics of cardiac allograft vasculopathy induced by immunomodulation in the miniature Swine.Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia · 2015
    Article
  19. Review
  20. Functional characterization of late outgrowth endothelial progenitor cells in patients with end-stage renal failure.Transplant international : official journal of the European Society for Organ Transplantation · 2014
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 3 countries.

J L HillebrandsDepartment of Cell Biology, Immunology Section, University of Groningen, The Netherlands.
F A Klatter
B M van den Hurk
E R Popa
P Nieuwenhuis
J Rozing
Regenerative Medicine Institute · MXUniversity of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of transplant arteriosclerosis (TA) is today's most important problem in clinical organ transplantation. Histologically, TA is characterized by perivascular inflammation and progressive intimal thickening. Current thought on this process of vascular remodeling assumes that neointimal vascular smooth muscle (VSM) cells and endothelium in TA are graft-derived, holding that medial VSM cells proliferate and migrate into the subendothelial space in response to signals from inflammatory cells and damaged graft endothelium. Using MHC class I haplotype-specific immunohistochemical staining and single-cell PCR analyses, we show that the neointimal alpha-actin-positive VSM cells in rat aortic or cardiac allografts are of recipient and not of donor origin. In aortic but not in cardiac allografts, recipient-derived endothelial cells (ECs) replaced donor endothelium. Cyclosporine treatment prevents neointima formation and preserves the vascular media in aortic allografts. Recipient-derived ECs do not replace graft endothelium after cyclosporine treatment. We propose that, although it progresses beyond the needs of functional repair, TA reflects the activity of a normal healing process that restores vascular wall function following allograft-induced immunological injury.

Indexed as

ActinsAnimalsAortaArteriosclerosisCyclosporineFemaleGenes, MHC Class IHeart TransplantationHumansImmunohistochemistryImmunosuppressive AgentsMaleMuscle, Smooth, VascularPolymerase Chain ReactionRatsRats, Inbred StrainsActinsCyclosporineImmunosuppressive Agents

Identifiers

PMID11390423
PMCPMC209313
OpenAlexW2041977741

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.