Evidence map›Paper›PMID 28122008›Full record

ArticlePloS one2017

Compromised Neurotrophic and Angiogenic Regenerative Capability during Tendon Healing in a Rat Model of Type-II Diabetes.

Aisha S Ahmed, Jian Li, Alim M D Abdul, Mahmood Ahmed, Claes-Göran Östenson, Paul T Salo, Carolyn Hewitt, David A Hart, Paul W Ackermann

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  5. Review
  6. Metabolic Syndrome and Tendon Disease: A Comprehensive Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
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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

9 authors at 4 institutions in 2 countries.

Aisha S AhmedKarolinska Institutet, Department of Clinical Neuroscience, Stockholm, Sweden.
Jian LiKarolinska Institutet, Department of Molecular Medicine and Surgery, Karolinska University Hospital, Solna, Stockholm, Sweden.
Alim M D AbdulKarolinska Institutet, Department of Molecular Medicine and Surgery, Karolinska University Hospital, Solna, Stockholm, Sweden.
Mahmood AhmedKarolinska Institutet, Department of Neurobiology, Care Sciences and Society, Center for Family and Community Medicine (CeFAM), Huddinge, Sweden.
Claes-Göran ÖstensonKarolinska Institutet, Department of Molecular Medicine and Surgery, Karolinska University Hospital, Solna, Stockholm, Sweden.
Paul T SaloMcCaig Institute for Bone & Joint Health, University of Calgary, Calgary, AB, Canada.
Carolyn HewittMcCaig Institute for Bone & Joint Health, University of Calgary, Calgary, AB, Canada.
David A HartMcCaig Institute for Bone & Joint Health, University of Calgary, Calgary, AB, Canada.
Paul W AckermannKarolinska Institutet, Department of Molecular Medicine and Surgery, Karolinska University Hospital, Solna, Stockholm, Sweden.
Karolinska Institutet · SEAlberta Bone and Joint Health Institute · CAKarolinska University Hospital · SEUniversity of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic diseases such as diabetes mellitus type-II (DM-II) may increase the risk of suffering painful connective tissue disorders and tendon ruptures. The pathomechanisms, however, by which diabetes adversely affects connective tissue matrix metabolism and regeneration, still need better definition. Our aim was to study the effect of DM-II on expressional changes of neuro- and angiotrophic mediators and receptors in intact and healing Achilles tendon. The right Achilles tendon was transected in 5 male DM-II Goto-Kakizaki (GK) and 4 age-matched Wistar control rats. The left Achilles tendons were left intact. At week 2 post-injury, NGF, BDNF, TSP, and receptors TrkA, TrkB and Nk1 gene expression was studied by quantitative RT-PCR (qRT-PCR) and their protein distribution by immunohistochemistry in intact and injured tendons. The expression of tendon-related markers, Scleraxis (SCX) and Tenomodulin (TNMD), was evaluated by qRT-PCR in intact and injured tendons. Injured tendons of diabetic GK rats exhibited significantly down-regulated Ngf and Tsp1 mRNA and corresponding protein levels, and down-regulated Trka gene expression compared to injured Wistar controls. Intact tendons of DM-II GK rats displayed reduced mRNA levels for Ngf, Tsp1 and Trkb compared to corresponding intact non-diabetic tendons. Up-regulated Scx and Tnmd gene expression was observed in injured tendons of normal and diabetic GK rats compared to intact Wistar controls. However, these molecules were not up-regulated in injured DM-II GK rats compared to their corresponding controls. Our results suggest that DM-II has detrimental effects on neuro- and angiotrophic pathways, and such effects may reflect the compromised repair seen in diabetic Achilles tendon. Thus, novel approaches for regeneration of injured, including tendinopathic, and surgically repaired diabetic tendons may include therapeutic molecular modulation of neurotrophic pathways such as NGF and its receptors.

Indexed as

Achilles TendonAnimalsBrain-Derived Neurotrophic FactorDiabetes Mellitus, Type 2Disease Models, AnimalGene ExpressionMaleNeovascularization, PhysiologicNerve Growth FactorRatsRats, WistarReceptors, Neurokinin-1Receptor, trkAReceptor, trkBSubstance PTendon InjuriesBrain-Derived Neurotrophic FactorNerve Growth FactorReceptors, Neurokinin-1Receptor, trkAReceptor, trkBSubstance P

Identifiers

PMID28122008
PMCPMC5266316
OpenAlexW2580870963

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.