ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
The Composite Antiadhesion Barrier Facilitated Fibroblast Autophagy Activation for Tendon Repair.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Recent advances in tendon redox biology: the interplay of oxidative stress, calcium signaling, and antioxidant defence mechanisms.Frontiers in pharmacology · 2026Review
- The Composite Antiadhesion Barrier Facilitated Fibroblast Autophagy Activation for Tendon Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
While dysregulated autophagy is implicated in fibrotic processes in various organs, its specific role in peritendinous fibrosis and tendon adhesion formation remains to be elucidated. This study hypothesizes that autophagy exerts a protective effect, inhibiting adhesion formation following tendon injury. Furthermore, it is proposed that interleukin-37 (IL-37) can be a potential therapeutic target for preventing tendon adhesions through autophagy activation. Therefore, an innovative three-layer composite antiadhesion barrier (pDNA@E-H-E') equipped with on-demand and unidirectional delivery strategy of bioactive plasmid DNA (pDNA) for IL-37 overexpression is designed. The novel finding of the fibroblast's autophagy activity as a protective factor in tendon adhesion highlights the encapsulation of IL-37-encoding pDNA nanocomposites in barrier for reaching supreme antiadhesion efficacy. Moreover, the reactive-oxygen-species-responsive and releasing-direction-guided pDNA@E-H-E' membranes afford wonderful inhibition of fibroblast proliferation, fibroblast-to-myofibroblast differentiation, and collagen synthesis by enhancing autophagy. Further in a rat Achilles tendon adhesion model, pDNA@E-H-E' membranes also significantly suppress peritendinous adhesion formation on the repaired sites and promote the scarless repair of Achilles tendon with optimum efficiency. In all, this study provides a promising approach for preventing tendon adhesion by employing a composite barrier with on-demand and unidirectional delivery strategy.
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Registered trials
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.