Evidence map›Paper›PMID 29373656›Full record

ReviewCardiovascular research2018

Role of smooth muscle cells in coronary artery bypass grafting failure.

Kerry Wadey, Joshua Lopes, Michelle Bendeck, Sarah George

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
9.2field-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

56 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Mechanical Activation of cPLA2 Impedes Fatty Acid β-Oxidation in Vein Grafts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. 3D Printing Approaches to Engineer Cardiac Tissue.Current cardiology reports · 2023
    Review
  20. 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

4 authors at 2 institutions in 2 countries.

Kerry WadeyBristol Medical School, Research Floor Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK.
Joshua LopesTranslational Biology and Engineering Program, University of Toronto, Toronto, ON M5G 1M1, Canada.
Michelle BendeckTranslational Biology and Engineering Program, University of Toronto, Toronto, ON M5G 1M1, Canada.
Sarah GeorgeBristol Medical School, Research Floor Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK.
Bristol Royal Infirmary · GBUniversity of Toronto · CA

Funding

British Heart Foundation FS/10/58/28515British Heart Foundation FS/17/46/33121British Heart Foundation PG/15/43/31567British Heart Foundation PG/17/66/33216CIHR MOP126042
6 · The paper itself

Abstract

Atherosclerosis is the underlying pathology of many cardiovascular diseases. The formation and rupture of atherosclerotic plaques in the coronary arteries results in angina and myocardial infarction. Venous coronary artery bypass grafts are designed to reduce the consequences of atherosclerosis in the coronary arteries by diverting blood flow around the atherosclerotic plaques. However, vein grafts suffer a high failure rate due to intimal thickening that occurs as a result of vascular cell injury and activation and can act as 'a soil' for subsequent atherosclerotic plaque formation. A clinically-proven method for the reduction of vein graft intimal thickening and subsequent major adverse clinical events is currently not available. Consequently, a greater understanding of the underlying mechanisms of intimal thickening may be beneficial for the design of future therapies for vein graft failure. Vein grafting induces inflammation and endothelial cell damage and dysfunction, that promotes vascular smooth muscle cell (VSMC) migration, and proliferation. Injury to the wall of the vein as a result of grafting leads to the production of chemoattractants, remodelling of the extracellular matrix and cell-cell contacts; which all contribute to the induction of VSMC migration and proliferation. This review focuses on the role of altered behaviour of VSMCs in the vein graft and some of the factors which critically lead to intimal thickening that pre-disposes the vein graft to further atherosclerosis and re-occurrence of symptoms in the patient.

Indexed as

AnimalsCell MovementCell ProliferationCoronary Artery BypassGraft Occlusion, VascularHumansMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaPhenotypeRisk FactorsSaphenous VeinSignal TransductionTreatment FailureVascular Remodeling

Identifiers

PMID29373656
PMCPMC5852543
OpenAlexW2789473108

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.