ArticleFrontiers in bioengineering and biotechnology2022
Disulfiram Suppressed Peritendinous Fibrosis Through Inhibiting Macrophage Accumulation and Its Pro-inflammatory Properties in Tendon Bone Healing.
Article in Frontiers in bioengineering and biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 14 citations in OpenAlex.
- Didymin may Enhance Tendon-Bone Healing Partly by Promoting PPAR-Mediated Fatty Acid Oxidation and Macrophage M2 Polarization.Immunity, inflammation and disease · 2026Article
- Exosomes derived from BMSCs regulate macrophage M1/M2 polarization and promoting tendon-bone healing through circRNA1052.Stem cell research & therapy · 2026Article
- Disulfiram attenuates immobilization-induced knee joint contracture by suppressing Caspase-1/GSDMD-mediated pyroptosis.Scientific reports · 2026Article
- Macrophage polarisation under immune regulation as a therapeutic target for tendon-bone healing: multifactorial regulation and mechanistic insights.Frontiers in immunology · 2026Review
- Multidimensional biomimetic strategy integrating structural, functional and biological cues for enhanced tendon-to-bone interface regeneration.Materials today. Bio · 2025Article
- Targeting pyroptosis in myocardial inflammation and fibrosis: molecular mechanisms and therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2025Review
- Healing of tendon-related diseases: insights from macrophage regulation.Military Medical Research · 2025Review
- Inflammatory Cell Interactions in the Rotator Cuff Microenvironment: Insights From Single-Cell Sequencing.International journal of genomics · 2025Review
- Mesenchymal stem cell-derived extracellular vesicles: a regulator and carrier for targeting bone-related diseases.Cell death discovery · 2024Review
- Inhibitors of the NLRP3 inflammasome pathway as promising therapeutic candidates for inflammatory diseases (Review).International journal of molecular medicine · 2023Review
- Parishin A-loaded mesoporous silica nanoparticles modulate macrophage polarization to attenuate tendinopathy.NPJ Regenerative medicine · 2023Article
- Mesenchymal stem cells and macrophages and their interactions in tendon-bone healing.Journal of orthopaedic translation · 2023Review
- Therapeutic potential and mechanisms of mesenchymal stem cell-derived exosomes as bioactive materials in tendon-bone healing.Journal of nanobiotechnology · 2023Review
- Regulating Macrophages through Immunomodulatory Biomaterials Is a Promising Strategy for Promoting Tendon-Bone Healing.Journal of functional biomaterials · 2022Review
- The repositioned drugs disulfiram/diethyldithiocarbamate combined to benznidazole: Searching for Chagas disease selective therapy, preventing toxicity and drug resistance.Frontiers in cellular and infection microbiology · 2022Article
- Transcriptomic Profiling Reveals NF-κB-Associated Immune Regulatory Signatures Underlying the Regenerative Effects of Hypoxia-Preconditioned Tendon Stem Cell-Derived Extracellular Vesicles.BioFactors (Oxford, England)Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The communication between macrophages and tendon cells plays a critical role in regulating the tendon-healing process. However, the potential mechanisms through which macrophages can control peritendinous fibrosis are unknown. Our data showed a strong pro-inflammatory phenotype of macrophages after a mouse tendon-bone injury. Moreover, by using a small-molecule compound library, we identified an aldehyde dehydrogenase inhibitor, disulfiram (DSF), which can significantly promote the transition of macrophage from M1 to M2 phenotype and decrease macrophage pro-inflammatory phenotype. Mechanistically, DSF targets gasdermin D (GSDMD) to attenuate macrophage cell pyroptosis, interleukin-1β, and high mobility group box 1 protein release. These pro-inflammatory cytokines and damage-associated molecular patterns are essential for regulating tenocyte and fibroblast proliferation, migration, and fibrotic activity. Deficiency or inhibition of GSDMD significantly suppressed peritendinous fibrosis formation around the injured tendon and was accompanied by increased regenerated bone and fibrocartilage compared with the wild-type littermates. Collectively, these findings reveal a novel pathway of GSDMD-dependent macrophage cell pyroptosis in remodeling fibrogenesis in tendon-bone injury. Thus, GSDMD may represent a potential therapeutic target in tendon-bone healing.
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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.