Evidence map›Paper›PMID 34869956›Full record

ReviewJACC. Basic to translational science2021

Animal Models of Neointimal Hyperplasia and Restenosis: Species-Specific Differences and Implications for Translational Research.

Max L A Ebert, Vanessa F Schmidt, Lena Pfaff, Anne von Thaden, Melanie A Kimm, Moritz Wildgruber

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in JACC. Basic to translational science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06782100 (MRI Guided Management of Occlusive Peripheral Arterial Disease), which is not on this map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-weighted citation impact, top 9% 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.

NCT06782100 recruitingnot on this mapstarted 2024, after this paper: background citation

MRI Guided Management of Occlusive Peripheral Arterial Disease

Typeobservational_patient_registrySponsorThe Methodist Hospital Research InstituteRan2024 to 2029Enrolled175ConditionsPeripheral Vascular Diseases
3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Tenascin CNature communications · 2026
    Article
  8. Review
  9. Article
  10. Development of a Novel Murine Model of In-Stent Neoatherosclerosis.Journal of the American Heart Association · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

6 authors at 2 institutions in 1 country.

Max L A EbertDepartment for Radiology, University Hospital, Ludwigs Maximilian University (LMU), Munich, Germany.
Vanessa F SchmidtDepartment for Radiology, University Hospital, Ludwigs Maximilian University (LMU), Munich, Germany.
Lena PfaffBiomedical Center Munich, Ludwigs Maximilian University (LMU), Munich, Germany.
Anne von ThadenGerman Center for Neurodegenerative Diseases, Ludwigs Maximilian University (LMU), Munich, Germany.
Melanie A KimmDepartment for Radiology, University Hospital, Ludwigs Maximilian University (LMU), Munich, Germany.
Moritz WildgruberDepartment for Radiology, University Hospital, Ludwigs Maximilian University (LMU), Munich, Germany.
Ludwig-Maximilians-Universität München · DEGerman Center for Neurodegenerative Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The process of restenosis is based on the interplay of various mechanical and biological processes triggered by angioplasty-induced vascular trauma. Early arterial recoil, negative vascular remodeling, and neointimal formation therefore limit the long-term patency of interventional recanalization procedures. The most serious of these processes is neointimal hyperplasia, which can be traced back to 4 main mechanisms: endothelial damage and activation; monocyte accumulation in the subintimal space; fibroblast migration; and the transformation of vascular smooth muscle cells. A wide variety of animal models exists to investigate the underlying pathophysiology. Although mouse models, with their ease of genetic manipulation, enable cell- and molecular-focused fundamental research, and rats provide the opportunity to use stent and balloon models with high throughput, both rodents lack a lipid metabolism comparable to humans. Rabbits instead build a bridge to close the gap between basic and clinical research due to their human-like lipid metabolism, as well as their size being accessible for clinical angioplasty procedures. Every different combination of animal, dietary, and injury model has various advantages and disadvantages, and the decision for a proper model requires awareness of species-specific biological properties reaching from vessel morphology to distinct cellular and molecular features.

Indexed as

angioplastyanimal modelApo, apolipoproteinCETP, cholesteryl ester transferase proteinECM, extracellular matrixFGF, fibroblast growth factorHDL, high-density lipoproteinLDL, low-density lipoproteinLDLr, LDL receptorneointimal hyperplasiaPDGF, platelet-derived growth factorrestenosisTGF, transforming growth factorVLDL, very low-density lipoproteinVSMC, vascular smooth muscle cell

Identifiers

PMID34869956
PMCPMC8617545
OpenAlexW3188806041

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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.