ArticleScientific reports2019
Deletion of NFKB1 enhances canonical NF-κB signaling and increases macrophage and myofibroblast content during tendon healing.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 86 citations in OpenAlex.
- Multi-omics-guided targeting of the CD14-NF-κB axis with PGA1-loaded liposomes restores CD14Materials today. Bio · 2026Article
- Mice lacking NF-ĸB1 undergo premature ovarian aging.Reproductive biology and endocrinology : RB&E · 2026Article
- Screening macrophage polarization genes in spinal cord injury as therapeutic targets.PloS one · 2026Article
- The mechanosensitive channel TRPV4 inhibits pulmonary inflammation by limiting NF-κB signaling in alveolar macrophages.Science signaling · 2025Article
- Nociceptive sensory neuron-derived NGF orchestrates a fibrotic mesenchymal stromal cell neurogenic niche to drive tendon pathological fibrosis.Nature communications · 2025Article
- Regenerative biologics modulating inflammation and promoting tenogenesis in equine superficial digital flexor tendonitis: from molecular pathways to clinical translation.Irish veterinary journal · 2025Review
- Epitenon-derived progenitors drive fibrosis and regeneration after flexor tendon injury in a spatially-dependent manner.Nature communications · 2025Article
- Functional tendon regeneration is driven by regulatory T cells and IL-33 signaling.Science advances · 2025Article
- Deciphering the pharmacological mechanism of Radix astragali for allergic rhinitis through network pharmacology and experimental validation.Scientific reports · 2024Article
- High-Temperature-Induced Differential Expression of miRNA Mediates Liver Inflammatory Response in Tsinling Lenok Trout (Brachymystax lenok tsinlingensis).Marine biotechnology (New York, N.Y.) · 2024Article
- Equine Embryonic Stem Cell-Derived Tenocytes are Insensitive to a Combination of Inflammatory Cytokines and Have Distinct Molecular Responses Compared to Primary Tenocytes.Stem cell reviews and reports · 2024Article
- Microbial Dynamics in Ophthalmic Health: Exploring the Interplay between Human Microbiota and Glaucoma Pathogenesis.Medicina (Kaunas, Lithuania) · 2024Review
- Interfacial Tissue Regeneration with Bone.Current osteoporosis reports · 2024Review
- Neuromorphic electro-stimulation based on atomically thin semiconductor for damage-free inflammation inhibition.Nature communications · 2024Article
- Understanding Fibrous Tissue in the Effective Healing of Rotator Cuff Injury.Journal of surgery and research · 2024Article
- Challenges in tendon-bone healing: emphasizing inflammatory modulation mechanisms and treatment.Frontiers in endocrinology · 2024Review
- The roles and mechanisms of the NF-κB signaling pathway in tendon disorders.Frontiers in veterinary science · 2024Review
- High-Dose Vitamin B6 (Pyridoxine) Displays Strong Anti-Inflammatory Properties in Lipopolysaccharide-Stimulated Monocytes.Biomedicines · 2023Article
- A frog peptide provides new strategies for the intervention against skin wound healing.Cellular & molecular biology letters · 2023Article
- Nanoscale vibration could promote tenogenic differentiation of umbilical cord mesenchymal stem cells.In vitro cellular & developmental biology. Animal · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Flexor tendon injuries heal with excessive scar tissue that limits range of motion and increases incidence of re-rupture. The molecular mechanisms that govern tendon healing are not well defined. Both the canonical nuclear factor kappa B (NF-κB) and mitogen activated protein kinase (MAPK) pathways have been implicated in tendon healing. The gene NFKB1 (proteins p105/p50) is involved in both NF-κB and MAPK signaling cascades. In the present study, we tested the hypothesis that global NFKB1 deletion would increase activation of both NF-κB and MAPK through loss of signaling repressors, resulting in increased matrix deposition and altered biomechanical properties. As hypothesized, NFKB1 deletion increased activation of both NF-κB and MAPK signaling. While gliding function was not affected, NFKB1 deletion resulted in tendons that were significantly stiffer and trending towards increased strength by four weeks post-repair. NFKB1 deletion resulted in increased collagen deposition, increase macrophage recruitment, and increased presence of myofibroblasts. Furthermore, NFKB1 deletion increased expression of matrix-related genes (Col1a1, Col3a1), macrophage-associated genes (Adgre1, Ccl2), myofibroblast markers (Acta2), and general inflammation (Tnf). Taken together, these data suggest that increased activation of NF-κB and MAPK via NFKB1 deletion enhance macrophage and myofibroblast content at the repair, driving increased collagen deposition and biomechanical properties.
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