Evidence mapPaperPMID 39726182Full record

ArticleJournal of anatomy2026

Achilles tenocytes from diabetic and non diabetic donors exposed to hyperglycemia respond differentially to inflammatory stimuli and stretch.

Nils Fleischmann, Sarah Hofmann, Clemens Gögele, Eva Frank, Christian Werner, Maria Kokozidou, Bernd Hoffmann, Jens Konrad, Gundula Schulze-Tanzil

Abstract read
In one paragraph

Article in Journal of anatomy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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

2 citing papers in PubMed.

  1. Article
  2. Tendon mechanobiology in the context of tendon biofabrication.Frontiers in bioengineering and biotechnology · 2025
    Review
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.

Nils FleischmannInstitute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg, Germany.
Sarah HofmannInstitute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg, Germany.
Clemens GögeleInstitute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg, Germany.ORCID https://orcid.org/0000-0002-7086-9743
Eva FrankInstitute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg, Germany.
Christian WernerInstitute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg, Germany.
Maria KokozidouInstitute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg, Germany.
Bernd HoffmannInstitute of Biological Information Processing, IBI-2: Mechanobiology, Research Centre Juelich, Juelich, Germany.
Jens KonradInstitute of Biological Information Processing, IBI-2: Mechanobiology, Research Centre Juelich, Juelich, Germany.
Gundula Schulze-TanzilInstitute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg, Germany.ORCID https://orcid.org/0000-0002-9807-9532

Funding

Deutsche Forschungsgemeinschaft SCHU1979/14-1Kerscher'sche Diabetes Research Foundation SZ_FP_008.18Kerscher'sche Diabetes Research Foundation SZ_FP_164.20
6 · The paper itself

Abstract

Diabetes mellitus type 2 (DMT2) promotes Achilles tendon (AS) degeneration and exercise could modulate features of DMT2. Hence, this study investigated whether tenocytes of non DMT2 and DMT2 rats respond differently to normo- (NG) and hyperglycemic (HG) conditions in the presence of tumor necrosis factor (TNF)α or cyclic stretch. AS tenocytes, isolated from DMT2 (fa/fa) or non DMT2 (lean, fa/+) adult Zucker Diabetic Fatty (ZDF) rats, were treated with 10 ng/mL TNFα either under NG or HG conditions (1 g/L vs. 4.5 g/L glucose) and were exposed to cyclic stretch (14%, 0.3 Hz, 48 h). Tenocyte survival, metabolic activity, gene and/or protein expression of tendon extracellular matrix component collagen type 1, alpha smooth muscle actin (αSMA, Acta2), the stress defense enzyme heme oxygenase-1 (Hmox1) as well as suppressors of cytokine signaling (Socs)1 and Socs3 were analyzed. Tenocyte vitality remained high, but metabolic activity was slightly impaired by HG conditions irrespectively of cell origin. Collagen type 1 alpha protein and gene expression was suppressed by TNFα, but only in cells of non DMT2 animals in NG culture medium. Higher amounts of αSMA were visualized in tendons/tenocytes of diabetic rats or those exposed to TNFα. Cyclic stretch caused cell alignment in zero stretch direction. In addition, it led to a significant reduction of cell perimeters, particularly in cells of DMT2 donor rats under HG conditions. Hmox1, Socs1 and Socs3 were induced by HG, but only in tenocytes of diabetic rats (4 h). Stretch induced significantly Hmox1 transcriptional activity under NG conditions and Socs3 under HG conditions especially in tenocytes of DMT2 rats. The response of tenocytes to TNFα and cyclic stretch depends on glucose supply and origin suggesting their irreversible impairment by DMT2.

Indexed as

Achilles TendonDiabetes Mellitus, Type 2HyperglycemiaInflammationTenocytesAnimalsMaleRatsRats, ZuckerStress, MechanicalTumor Necrosis Factor-alphaTumor Necrosis Factor-alphaAchilles tendoncyclic stretchcytokinediabetes mellitus type 2tendinopathytenocytesTNFα

Identifiers

PMID39726182
PMCPMC13140746

What Socratic holds

Textmetadata
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Registered trials

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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 Socratic graph.