Evidence map›Paper›PMID 23576636›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Chronic kidney disease accelerates endothelial barrier dysfunction in a mouse model of an arteriovenous fistula.

Anlin Liang, Yun Wang, Guofeng Han, Luan Truong, Jizhong Cheng

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

43 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. A Vein Attempt? Experimental Models for Arteriovenous Fistula Research.Cardiovascular engineering and technology · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. The rodent models of arteriovenous fistula.Frontiers in cardiovascular medicine · 2024
    Review
  7. Article
  8. Article
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  12. Review
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  19. Review
  20. c-Kit suppresses atherosclerosis in hyperlipidemic mice.American journal of physiology. Heart and circulatory physiology · 2019
    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 1 institution in 2 countries.

Anlin LiangDivision of Nephrology, Baylor College of Medicine, Houston, TX 77030, USA.
Yun Wang
Guofeng Han
Luan Truong
Jizhong Cheng
Baylor College of Medicine · US

Funding

PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR01DK037175 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI Zhaoyong Hu · 1986 to 2026
$4.3M
PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR37DK037175 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2006 to 2015
$3.8M
CHRONIC KIDNEY DISEASE ADVERSELY INFLUENCES VASCULAR FUNCTIONSR01DK095867 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHENG, JIZHONG · 2013 to 2017
$1.7M
NIDDK NIH HHS DK-37175NIDDK NIH HHS R01 DK095867NIDDK NIH HHS R01-DK095867
6 · The paper itself

Abstract

Hemodialysis patients depend on arteriovenous fistulas (AVF) for vascular access. Unfortunately, their 2-yr primary patency rate is only 60% because of AVF clog due to intimal hyperplasia at the venous anastomosis. Chronic kidney disease (CKD) can increase neointima formation by unknown mechanisms. A new AVF mouse model was created, and the mechanisms of CKD on neointima formation in AVFs were investigated. We created AVFs in mice by anastomosing the common carotid artery to the internal jugular vein. CKD was induced [BUN (blood urea nitrogen) in control and CKD mice, 33.3 ± 3.9 vs. 114.2 ± 12.1 mg/dl, P < 0.05]. After 1 day, there was endothelial cell loss and CD41-positive platelet aggregation, especially in the venous anastomosis. An invasion of macrophages and neutrophils peaked at 1 wk after surgery. Neointima formation (smooth muscle cell accumulation and extracellular matrix deposition) increased progressively over 4 wk. Mice with CKD had ~45% (P < 0.05) more neointima formation than control mice. CKD decreased vascular endothelial-cadherin expression in endothelial cells and delayed regeneration of the endothelium. CKD also increased inflammatory cells (Mac-2-positive or CD45-positive) in AVFs at 2 wk. Finally, AVFs were "leakier" (increased accumulation of Evans blue) in CKD mice at 7 and 14 days than control mice. We find that CKD increases neointima formation and endothelial barrier dysfunction. We have created a mouse model of AVF with characteristics similar to failed AVFs in patients. The model will allow testing of strategies directed at improving AVF function in CKD patients.

Indexed as

Arteriovenous Shunt, SurgicalAnimalsArteriovenous FistulaCarotid Artery, CommonEndotheliumJugular VeinsMaleMiceMice, Inbred C57BLModels, AnimalNeointimaRenal Insufficiency, Chronicarteriovenous fistulachronic kidney diseaseendothelial barrierneointima

Identifiers

PMID23576636
PMCPMC3680675
OpenAlexW2155136404

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.