Evidence map›Paper›PMID 34830167›Full record

ArticleInternational journal of molecular sciences2021

Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention.

Jenq-Shyong Chan, Yang Wang, Virgilius Cornea, Prabir Roy-Chaudhury, Begoña Campos

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Molecular Mechanisms of Hemostasis, Thrombosis and Thrombo-Inflammation.International journal of molecular sciences · 2022
    Article
  3. 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

5 authors at 3 institutions in 2 countries.

Jenq-Shyong ChanDivision of Nephrology, Department of Internal Medicine, Armed Forces Taoyuan General Hospital, Taoyuan 325, Taiwan.ORCID 0000-0003-2791-0162
Yang WangDivision of Nephrology, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH 45267, USA.
Virgilius CorneaDepartment of Pathology, University of Cincinnati, Cincinnati, OH 45267, USA.
Prabir Roy-ChaudhuryDepartment of Medicine, Division of Nephrology and Hypertension, University of North Carolina, Chapel Hill, NC 27599, USA.
Begoña CamposDivision of Nephrology, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH 45267, USA.
University of Cincinnati · USTri-Service General Hospital · TWUniversity of North Carolina at Chapel Hill · US

Funding

Dr. Roy- 309 Chaudhury. Dr. Roy-Chaudhury USA VA Merit Award [1I01BX002390-01]The National Institutes of Health, USA [R44AG059279 and R41HL151235]
6 · The paper itself

Abstract

backgroundArteriovenous fistula (AVF) stenosis remains an important cause of AVF maturation failure, for which there are currently no effective therapies. We examined the pattern and phenotype of cellular proliferation at different timepoints in a mouse model characterized by a peri-anastomotic AVF stenosis.

methodsStandard immunohistochemical analyses for cellular proliferation and macrophage infiltration were performed at 2, 7 and 14 d on our validated mouse model of AVF stenosis to study the temporal profile, geographical location and cellular phenotype of proliferating and infiltrating cells in this model.

resultsAdventitial proliferation and macrophage infiltration (into the adventitia) began at 2 d, peaked at 7 d and then declined over time. Surprisingly, there was minimal macrophage infiltration or proliferation in the neointimal region at either 7 or 14 d, although endothelial cell proliferation increased rapidly between 2 d and 7 d, and peaked at 14 d.

conclusionsEarly and rapid macrophage infiltration and cellular proliferation within the adventitia could play an important role in the downstream pathways of both neointimal hyperplasia and inward or outward remodelling.

Indexed as

Cell ProliferationAdventitiaAnimalsConstriction, PathologicDisease Models, AnimalEndothelial CellsMacrophagesMiceNeointimaadventitiaarteriovenous fistulamacrophageproliferation

Identifiers

PMID34830167
PMCPMC8623099
OpenAlexW3214628607

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.