ArticleThe Journal of pathology2016
Interaction of TWEAK with Fn14 leads to the progression of fibrotic liver disease by directly modulating hepatic stellate cell proliferation.
Article in The Journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 64 citations in OpenAlex.
- A bio-fortified whole tomato food supplement as potential dietary tool for the management of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).Journal of translational medicine · 2026Article
- Liver Progenitor Cells: Cellular Origins, Plasticity, and Signaling Pathways in Liver Regeneration.Biology · 2025Review
- Single-cell RNA sequencing advances in revealing the development and progression of MASH: the identifications and interactions of non-parenchymal cells.Frontiers in molecular biosciences · 2025Review
- Relationship between Genes and microRNAs Involved in the Migration of Cells from the Bone Marrow during Experimental Liver Fibrosis.Bulletin of experimental biology and medicine · 2025Article
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- Fn14 and TNFR2 as regulators of cytotoxic TNFR1 signaling.Frontiers in cell and developmental biology · 2023Review
- Clinical and laboratory characterization of patients with localized scleroderma and response to UVA-1 phototherapy: In vivo and in vitro skin models.Photodermatology, photoimmunology & photomedicine · 2022Article
- Advances of cancer-associated fibroblasts in liver cancer.Biomarker research · 2022Review
- Fn14 exacerbates acute lung injury by activating the NLRP3 inflammasome in mice.Molecular medicine (Cambridge, Mass.) · 2022Article
- The TWEAK/Fn14/CD163 axis-implications for metabolic disease.Reviews in endocrine & metabolic disorders · 2022Review
- Revealing potential anti-fibrotic mechanism of Ganxianfang formula based on RNA sequence.Chinese medicine · 2022Article
- FN14 mRNA Expression Correlates with an Increased Number of Veins during Angiogenesis in the Process of Liver Fibrosis.International journal of molecular and cellular medicine · 2022Article
- TNF-α induces endothelial-mesenchymal transition promoting stromal development of pancreatic adenocarcinoma.Cell death & disease · 2021Article
- Single-cell technologies in hepatology: new insights into liver biology and disease pathogenesis.Nature reviews. Gastroenterology & hepatology · 2020Review
- Molecular Profiling Reveals a Common Metabolic Signature of Tissue Fibrosis.Cell reports. Medicine · 2020Article
- Fn14 Participates in Neuropathic Pain Through NF-κB Pathway in Primary Sensory Neurons.Molecular neurobiology · 2019Article
- Soluble Tumor Necrosis Factor Like Weak Inducer of Apoptosis and Vitamin D in Hemodialysis Patients: Relation to Carotid Intima-Media Thickness.Indian journal of clinical biochemistry : IJCB · 2018Article
- Tumor necrosis factor-like weak inducer of apoptosis induces inflammation in Graves' orbital fibroblasts.PloS one · 2018Article
- Article
- Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice.Journal of immunology research · 2018Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Tumour necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) have been associated with liver regeneration in vivo. To further investigate the role of this pathway we examined their expression in human fibrotic liver disease and the effect of pathway deficiency in a murine model of liver fibrosis. The expression of Fn14 and TWEAK in normal and diseased human and mouse liver tissue and primary human hepatic stellate cells (HSCs) were investigated by qPCR, western blotting and immunohistochemistry. In addition, the levels of Fn14 in HSCs following pro-fibrogenic and pro-inflammatory stimuli were assessed and the effects of exogenous TWEAK on HSCs proliferation and activation were studied in vitro. Carbon tetrachloride (CCl4 ) was used to induce acute and chronic liver injury in TWEAK KO mice. Elevated expression of both Fn14 and TWEAK were detected in acute and chronic human liver injury, and co-localized with markers of activated HSCs. Fn14 levels were low in quiescent HSCs but were significantly induced in activated HSCs, which could be further enhanced with the profibrogenic cytokine TGFβ in vitro. Stimulation with recombinant TWEAK induced proliferation but not further HSCs activation. Fn14 gene expression was also significantly up-regulated in CCl4 models of hepatic injury whereas TWEAK KO mice showed reduced levels of liver fibrosis following chronic CCl4 injury. In conclusion, TWEAK/Fn14 interaction leads to the progression of fibrotic liver disease via direct modulation of HSCs proliferation, making it a potential therapeutic target for liver fibrosis.
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