Evidence map›Paper›PMID 26915560›Full record

ArticleScientific reports2016

Role of Excessive Autophagy Induced by Mechanical Overload in Vein Graft Neointima Formation: Prediction and Prevention.

Ya-Ju Chang, Hui-Chun Huang, Yuan-Yu Hsueh, Shao-Wei Wang, Fong-Chin Su, Chih-Han Chang, Ming-Jer Tang, Yi-Shuan Li, Shyh-Hau Wang, Kirk K Shung and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Ya-Ju ChangInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
Hui-Chun HuangInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
Yuan-Yu HsuehDivision of Plastic Surgery, National Cheng Kung University Hospital, Tainan, Taiwan.
Shao-Wei WangDepartment of Biomedical Engineering, National Cheng Kung University, Tainan, Taiwan.
Fong-Chin SuDepartment of Biomedical Engineering, National Cheng Kung University, Tainan, Taiwan.
Chih-Han ChangDepartment of Biomedical Engineering, National Cheng Kung University, Tainan, Taiwan.
Ming-Jer TangDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
Yi-Shuan LiInstitute of Engineering in Medicine, University of California, San Diego, CA92093, USA.
Shyh-Hau WangDepartment of Computational Science, National Cheng Kung University, Tainan, Taiwan.
Kirk K ShungDepartment of Biomedical Engineering, University of Southern California, Los Angeles, CA90089, USA.
Shu ChienInstitute of Engineering in Medicine, University of California, San Diego, CA92093, USA.
Chia-Ching WuInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
National Cheng Kung University · TWUniversity of California, San Diego · USNational Cheng Kung University Hospital · TWUniversity of Southern California · US

Funding

A Resource on Medical Ultrasonic Transducer TechnologyP41EB002182 · NIBIB · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SHUNG, K KIRK · 2003 to 2016
$13.3M
NIBIB NIH HHS P41 EB002182
6 · The paper itself

Abstract

Little is known regarding the interplays between the mechanical and molecular bases for vein graft restenosis. We elucidated the stenosis initiation using a high-frequency ultrasonic (HFU) echogenicity platform and estimated the endothelium yield stress from von-Mises stress computation to predict the damage locations in living rats over time. The venous-arterial transition induced the molecular cascades for autophagy and apoptosis in venous endothelial cells (ECs) to cause neointimal hyperplasia, which correlated with the high echogenicity in HFU images and the large mechanical stress that exceeded the yield strength. The ex vivo perfusion of arterial laminar shear stress to isolated veins further confirmed the correlation. EC damage can be rescued by inhibiting autophagy formation using 3-methyladenine (3-MA). Pretreatment of veins with 3-MA prior to grafting reduced the pathological increases of echogenicity and neointima formation in rats. Therefore, this platform provides non-invasive temporal spatial measurement and prediction of restenosis after venous-arterial transition as well as monitoring the progression of the treatments.

Indexed as

AdenineAnimalsApoptosisArteriesAutophagyEndothelial CellsGraft Occlusion, VascularNeointimaRatsRats, Sprague-DawleyStress, MechanicalVeins3-methyladenineAdenine

Identifiers

PMID26915560
PMCPMC4768319
OpenAlexW2398406629

What OpenQuestion holds

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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.