ArticleCureus2025
Elevation of NTN4 Expression and Its Possible Regulation by Tumor Necrosis Factor-Alpha (TNF-α) in a Rat Model of Rotator Cuff Tear.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- Prognostic and immunological implications of a mitophagy-associated gene signature in bladder cancer.Translational andrology and urology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionRotator cuff tears are a major cause of shoulder dysfunction and pain, particularly in older adults, with re-tear rates remaining high despite surgical advances. Persistent inflammation and dysregulated extracellular matrix (ECM) remodeling contribute to impaired healing. Tumor necrosis factor-α (TNF-α) is known to drive tendon inflammation, but the downstream mediators linking TNF-α signaling to matrix degradation remain incompletely understood. Netrin-4 (NTN4), a laminin-related protein, has been implicated in inflammatory and ECM-modulating processes. We hypothesized that NTN4 is upregulated following tendon tear in a TNF-α-dependent manner and contributes to sustained ECM degradation.
methodsA rat infraspinatus and supraspinatus full-thickness tendon tear model was established, and tendon tissues were harvested at 0 (intact), 7, 14, 28, and 56 days post-injury (n = 8/time point). Gene expressions of
resultsIn vivo,
conclusionsOur findings identify NTN4 as a TNF-α-induced effector that contributes to sustained MMP-3-mediated matrix degradation following rotator cuff tear. By linking inflammatory cytokine signaling to prolonged ECM remodeling, the TNF-α/NTN4/MMP-3 axis may represent a potential therapeutic target for improving tendon healing and reducing re-tear risk.
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Registered trials
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