Evidence map›Paper›PMID 25866325›Full record

ArticleVascular pharmacology2015

Improving arteriovenous fistula patency: Transdermal delivery of diclofenac reduces cannulation-dependent neointimal hyperplasia via AMPK activation.

Mark G MacAskill, David G Watson, Marie-Ann Ewart, Roger Wadsworth, Andrew Jackson, Emma Aitken, Graeme MacKenzie, David Kingsmore, Susan Currie, Paul Coats

Open access · hybridAbstract read
In one paragraph

Article in Vascular pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. A Vein Attempt? Experimental Models for Arteriovenous Fistula Research.Cardiovascular engineering and technology · 2026
    Review
  3. Evaluating Animal Models for Improved Hemodialysis Vascular Access: A Focus on Arteriovenous Fistula.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Review
  4. Article
  5. Article
  6. 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

10 authors at 3 institutions in 1 country.

Mark G MacAskillStrathclyde Institute of Pharmacy and Biomedical Science, University of Strathclyde Glasgow, UK.
David G WatsonStrathclyde Institute of Pharmacy and Biomedical Science, University of Strathclyde Glasgow, UK.
Marie-Ann EwartInstitute of Cardiovascular & Medical Sciences, University of Glasgow, UK.
Roger WadsworthStrathclyde Institute of Pharmacy and Biomedical Science, University of Strathclyde Glasgow, UK.
Andrew JacksonDepartment of Renal Surgery, Western Infirmary, Glasgow, UK.
Emma AitkenDepartment of Renal Surgery, Western Infirmary, Glasgow, UK.
Graeme MacKenzieStrathclyde Institute of Pharmacy and Biomedical Science, University of Strathclyde Glasgow, UK.
David KingsmoreDepartment of Renal Surgery, Western Infirmary, Glasgow, UK.
Susan CurrieStrathclyde Institute of Pharmacy and Biomedical Science, University of Strathclyde Glasgow, UK.
Paul CoatsStrathclyde Institute of Pharmacy and Biomedical Science, University of Strathclyde Glasgow, UK. Electronic address: paul.coats@strath.ac.uk.
University of Strathclyde · GBWestern Infirmary · GBUniversity of Glasgow · GB

Funding

Biotechnology and Biological Sciences Research Council
6 · The paper itself

Abstract

Creation of an autologous arteriovenous fistula (AVF) for vascular access in haemodialysis is the modality of choice. However neointimal hyperplasia and loss of the luminal compartment result in AVF patency rates of ~60% at 12months. The exact cause of neointimal hyperplasia in the AVF is poorly understood. Vascular trauma has long been associated with hyperplasia. With this in mind in our rabbit model of AVF we simulated cannulation autologous to that undertaken in vascular access procedures and observed significant neointimal hyperplasia as a direct consequence of cannulation. The neointimal hyperplasia was completely inhibited by topical transdermal delivery of the non-steroidal anti-inflammatory (NSAID) diclofenac. In addition to the well documented anti-inflammatory properties we have identified novel anti-proliferative mechanisms demonstrating diclofenac increases AMPK-dependent signalling and reduced expression of the cell cycle protein cyclin D1. In summary prophylactic transdermal delivery of diclofenac to the sight of AVF cannulation prevents adverse neointimal hyperplasic remodelling and potentially offers a novel treatment option that may help prolong AVF patency and flow rates.

Indexed as

Administration, CutaneousAMP-Activated Protein KinasesAnimalsArteriovenous FistulaCatheterizationCell ProliferationCells, CulturedDiclofenacDose-Response Relationship, DrugDrug Delivery SystemsEnzyme ActivationHyperplasiaNeointimaRabbitsVascular PatencyAMP-Activated Protein KinasesDiclofenacArteriovenous fistula VascularCell proliferationPharmacotherapyRe-stenosis

Identifiers

PMID25866325
PMCPMC4534710
OpenAlexW2073096462

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.