ArticleCell death & disease2018
Fn14 deficiency ameliorates psoriasis-like skin disease in a murine model.
Article in Cell death & disease, 2018. 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, 33 citations in OpenAlex.
- Research progress on TWEAK/Fn14 signaling in chronic wound healing.Frontiers in surgery · 2026Review
- Synergistic effects of LCN2 and TWEAK on the progression of psoriasis.Cellular & molecular immunology · 2025Article
- Curcumol attenuates hyperproliferation and inflammatory response in a psoriatic HaCaT keratinocyte model by inhibiting the PI3K-Akt pathway and ameliorates skin lesions and inflammatory status in psoriasis-like mice.Inflammopharmacology · 2025Article
- Engineered Mesenchymal Stem Cell-Derived Extracellular Vesicles Scavenge Self-Antigens for Psoriasis Therapy via Modulating Metabolic and Immunological Disorders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Single-cell RNA-seq and bulk-seq identify RAB17 as a potential regulator of angiogenesis by human dermal microvascular endothelial cells in diabetic foot ulcers.Burns & trauma · 2023Article
- Fn14 and TNFR2 as regulators of cytotoxic TNFR1 signaling.Frontiers in cell and developmental biology · 2023Review
- Proteolytically generated soluble Tweak Receptor Fn14 is a blood biomarker for γ-secretase activity.EMBO molecular medicine · 2022Article
- Exocyst inactivation in urothelial cells disrupts autophagy and activates non-canonical NF-κB signaling.Disease models & mechanisms · 2022Article
- TNFR2 Depletion Reduces Psoriatic Inflammation in Mice by Downregulating Specific Dendritic Cell Populations in Lymph Nodes and Inhibiting IL-23/IL-17 Pathways.The Journal of investigative dermatology · 2022Article
- Advances in the pathogenesis of psoriasis: from keratinocyte perspective.Cell death & disease · 2022Review
- TWEAK functions with TNF and IL-17 on keratinocytes and is a potential target for psoriasis therapy.Science immunology · 2021Article
- Inhibition of fibroblast growth factor-inducible 14 attenuates experimental tubulointerstitial fibrosis and profibrotic factor expression of proximal tubular epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- Experimental atopic dermatitis is dependent on the TWEAK/Fn14 signaling pathway.Clinical and experimental immunology · 2020Article
- Multi-omics profiling of calcium-induced human keratinocytes differentiation reveals modulation of unfolded protein response signaling pathways.Cell cycle (Georgetown, Tex.) · 2019Article
- Article
- Tumor Necrosis Factor (TNF) Receptor Expression Determines Keratinocyte Fate upon Stimulation with TNF-Like Weak Inducer of Apoptosis.Mediators of inflammation · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a multifunctional cytokine that acts through its receptor fibroblast growth factor-inducible 14 (Fn14). Recent studies demonstrated that the TWEAK/Fn14 signals participate in the development of psoriasis. The purpose of this study was to further explore the effect of Fn14 inhibition on experimental psoriasis. Psoriasis-like skin disease was induced in the wild-type and Fn14-knockout BALB/c mice. We found that Fn14 deficiency ameliorates psoriasis-like lesion in this model, accompanied by less inflammatory cell infiltration and proinflammatory cytokine production in lesional skin. The cutaneous expression of TNF receptor type 2 also decreased in the Fn14-deficient mice. Moreover, the topical application of TWEAK exacerbated psoriatic lesion in the wild-type but not in the Fn14-deficient mice. Furthermore, TWEAK promoted the expression of interleukin 8, keratin 17, and epidermal growth factor receptor (EGFR) but inhibited the expression of involucrin in psoriatic keratinocytes in vitro. Interestingly, such effect of TWEAK was abrogated by an EGFR inhibitor (erlotinib). TWEAK also enhances the proliferation and interleukin-6 production of dermal microvascular endothelial cells under psoriatic condition. In conclusion, TWEAK/Fn14 signals contribute to the development of psoriasis, and involves the modulation of resident cells and the transduction of the EGFR pathway. Fn14 inhibition might be a novel therapeutic strategy for patients with psoriasis.
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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 Socratic graph.