ArticleFrontiers in pharmacology2018
Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Research progress on TWEAK/Fn14 signaling in chronic wound healing.Frontiers in surgery · 2026Review
- Cold Atmospheric Plasma Enhances Fn14 Signaling in Hair Follicle Stem Cells, Thereby Promoting the Healing of Diabetic Skin Wounds in a Mouse Model.Journal of immunology research · 2026Article
- TWEAK increases angiogenesis to promote diabetic skin wound healing by regulating Fn14/EGFR signaling.Journal of cosmetic dermatology · 2024Article
- Methotrexate Mechanism of Action in Plaque Psoriasis: Something New in the Old View.The Journal of clinical and aesthetic dermatology · 2022Article
- Controversies in TWEAK-Fn14 signaling in skeletal muscle atrophy and regeneration.Cellular and molecular life sciences : CMLS · 2020Review
- Proinflammatory cytokines regulate epidermal stem cells in wound epithelialization.Stem cell research & therapy · 2020Review
- Burns Impair Blood-Brain Barrier and Mesenchymal Stem Cells Can Reverse the Process in Mice.Frontiers in immunology · 2020Article
- The Dynamics of the Skin's Immune System.International journal of molecular sciences · 2019Review
- Ginkgo Flavonol Glycosides or Ginkgolides Tend to Differentially Protect Myocardial or Cerebral Ischemia-Reperfusion InjuryFrontiers in pharmacology · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interaction of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor inducible 14 (Fn14) participates in inflammatory responses, fibrosis, and tissue remodeling, which are central in the repair processes of wounds. Fn14 is expressed in main skin cells including dermal fibroblasts. This study was designed to explore the therapeutic effect of TWEAK on experimental burn wounds and the relevant mechanism underlying such function. Third-degree burns were introduced in two BALB/c mouse strains. Recombinant TWEAK was administrated topically, followed by the evaluation of wound areas and histologic changes. Accordingly, the downstream cytokines, inflammatory cell infiltration, and extracellular matrix synthesis were examined in lesional tissue. Moreover, the differentiation markers were analyzed in cultured human dermal fibroblasts upon TWEAK stimulation. The results showed that topical TWEAK accelerated the healing of burn wounds in wild-type mice but not in Fn14-deficient mice. TWEAK strengthened inflammatory cell infiltration, and exaggerated the production of growth factor and extracellular matrix components in wound areas of wild-type mice. Moreover, TWEAK/Fn14 activation elevated the expression of myofibroblastic differentiation markers, including alpha-smooth muscle actin and palladin, in cultured dermal fibroblasts. Therefore, topical TWEAK exhibits therapeutic effect on experimental burn wounds through favoring regional inflammation, cytokine production, and extracellular matrix synthesis. TWEAK/Fn14 activation induces the myofibroblastic differentiation of dermal fibroblasts, partially contributing to the healing of burn wounds.
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