Evidence map›Paper›PMID 28266660›Full record

ArticleScientific reports2017

High glucose alters tendon homeostasis through downregulation of the AMPK/Egr1 pathway.

Yu-Fu Wu, Hsing-Kuo Wang, Hong-Wei Chang, Jingyu Sun, Jui-Sheng Sun, Yuan-Hung Chao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

48 citing papers in PubMed, 66 citations in OpenAlex.

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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

6 authors at 3 institutions in 2 countries.

Yu-Fu WuSchool and Graduate Institute of Physical Therapy, College of Medicine, National Taiwan University, Taipei, Taiwan.
Hsing-Kuo WangSchool and Graduate Institute of Physical Therapy, College of Medicine, National Taiwan University, Taipei, Taiwan.
Hong-Wei ChangNephrology Division, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Jingyu SunSports and Health Research Center, Tongji University Department of Physical Education, Shanghai, China.
Jui-Sheng SunDepartment of Orthopedic Surgery, College of Medicine, National Taiwan University, Taipei, Taiwan.
Yuan-Hung ChaoSchool and Graduate Institute of Physical Therapy, College of Medicine, National Taiwan University, Taipei, Taiwan.
National Taiwan University Hospital · TWNational Taiwan University · TWTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) is associated with higher risk of tendinopathy, which reduces tolerance to exercise and functional activities and affects lifestyle and glycemic control. Expression of tendon-related genes and matrix metabolism in tenocytes are essential for maintaining physiological functions of tendon. However, the molecular mechanisms involved in diabetic tendinopathy remain unclear. We hypothesized that high glucose (HG) alters the characteristics of tenocyte. Using in vitro 2-week culture of tenocytes, we found that expression of tendon-related genes, including Egr1, Mkx, TGF-β1, Col1a2, and Bgn, was significantly decreased in HG culture and that higher glucose consumption occurred. Down-regulation of Egr1 by siRNA decreased Scx, Mkx, TGF-β1, Col1a1, Col1a2, and Bgn expression. Blocking AMPK activation with Compound C reduced the expression of Egr1, Scx, TGF-β1, Col1a1, Col1a2, and Bgn in the low glucose condition. In addition, histological examination of tendons from diabetic mice displayed larger interfibrillar space and uneven glycoprotein deposition. Thus, we concluded that high glucose alters tendon homeostasis through downregulation of the AMPK/Egr1 pathway and the expression of downstream tendon-related genes in tenocytes. The findings render a molecular basis of the mechanism of diabetic tendinopathy and may help develop preventive and therapeutic strategies for the pathology.

Indexed as

Achilles TendonAMP-Activated Protein KinasesAnimalsDown-RegulationEarly Growth Response Protein 1GlucoseRatsRats, Sprague-DawleySignal TransductionTendinopathyTenocytesAMP-Activated Protein KinasesEarly Growth Response Protein 1Egr1 protein, ratGlucose

Identifiers

PMID28266660
PMCPMC5339827
OpenAlexW2591988798

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.