ReviewBritish journal of pharmacology2013
The TWEAK-Fn14 system as a potential drug target.
Review in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
53 citing papers in PubMed, 84 citations in OpenAlex.
- Research progress on TWEAK/Fn14 signaling in chronic wound healing.Frontiers in surgery · 2026Review
- Integrating multi-omics, EWAS, and reverse network toxicology to explore environmental pollutant risks in erectile dysfunction.Frontiers in cell and developmental biology · 2026Article
- Hyperthermia and Early Growth of Cerebral Infarct: The Potential Role of Blood-Brain Barrier Permeability.Translational stroke research · 2025Article
- TWEAK-Fn14: a promising target for cardio-cerebrovascular diseases and brain-heart syndrome.Frontiers in immunology · 2025Review
- The Oncogenic Role of TNFRSF12A in Colorectal Cancer and Pan-Cancer Bioinformatics Analysis.Cancer research and treatment · 2025Article
- Deciphering the Synthetic and Refolding Strategy of a Cysteine-Rich Domain in the Tumor Necrosis Factor Receptor (TNF-R) for Racemic Crystallography Analysis and d-Peptide Ligand Discovery.ACS bio & med chem Au · 2024Article
- Advancing Treatment in Bullous Pemphigoid: A Comprehensive Review of Novel Therapeutic Targets and Approaches.Clinical reviews in allergy & immunology · 2023Review
- Extracellular Vesicle-Associated TWEAK Contributes to Vascular Inflammation and Remodeling During Acute Cellular Rejection.JACC. Basic to translational science · 2023Article
- Expression and clinical significance of tumor necrosis factor receptor-associated factor 1 in peripheral blood of patients with advanced lung cancer.American journal of translational research · 2023Article
- Fn14 and TNFR2 as regulators of cytotoxic TNFR1 signaling.Frontiers in cell and developmental biology · 2023Review
- Antibody-based soluble and membrane-bound TWEAK mimicking agonists with FcγR-independent activity.Frontiers in immunology · 2023Article
- Proteolytically generated soluble Tweak Receptor Fn14 is a blood biomarker for γ-secretase activity.EMBO molecular medicine · 2022Article
- 3β-Hydroxy-5β-hydroxy-B-norcholestane-6β-carboxaldehyde (SEC-B) Induces Proinflammatory Activation of Human Endothelial Cells Associated with Nitric Oxide Production and Endothelial Nitric Oxide Synthase/Caveolin-1 Dysregulation.Antioxidants (Basel, Switzerland) · 2022Article
- Unlocking the gate to GABARAPL2.Biologia futura · 2022Review
- sTWEAK is a leukoaraiosis biomarker associated with neurovascular angiopathy.Annals of clinical and translational neurology · 2022Observational
- Targeting fibroblast growth factor (FGF)-inducible 14 (Fn14) for tumor therapy.Frontiers in pharmacology · 2022Review
- Diagnostic test accuracy of novel biomarkers for lupus nephritis-An overview of systematic reviews.PloS one · 2022Review
- sTWEAK is a marker of early haematoma growth and leukoaraiosis in intracerebral haemorrhage.Stroke and vascular neurology · 2021Observational
- Anti-Fn14 Antibody-Conjugated Nanoparticles Display Membrane TWEAK-Like Agonism.Pharmaceutics · 2021Article
- Identification of Pan-Cancer Biomarkers Based on the Gene Expression Profiles of Cancer Cell Lines.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor-inducible 14 (Fn14) is a member of the tumour necrosis factor (TNF) receptor family that is induced in a variety of cell types in situations of tissue injury. Fn14 becomes activated by TNF-like weak inducer of apoptosis (TWEAK), a typical member of the TNF ligand family. TWEAK is constitutively expressed by monocytes and some tumour cell lines and also shows cytokine inducible expression in various other cell types. Fn14 activation results in stimulation of signalling pathways culminating in the activation of NFκB transcription factors and various MAPKs but might also trigger the PI3K/Akt pathway and GTPases of the Rho family. In accordance with its tissue damage-associated expression pattern and its pleiotropic proinflammatory signalling capabilities, the TWEAK-Fn14 system has been implicated in a huge number of pathologies. The use of TWEAK- and Fn14-knockout mice identified the TWEAK-Fn14 system as a crucial player in muscle atrophy, cerebral ischaemia, kidney injury, atherosclerosis and infarction as well as in various autoimmune scenarios including experimental autoimmune encephalitis, rheumatoid arthritis and inflammatory bowel disease. Moreover, there is increasing preclinical evidence that Fn14 targeting is a useful option in tumour therapy. Based on a discussion of the signalling capabilities of TWEAK and Fn14, this review is focused on two major issues. On the one hand, on the molecular and cellular basis of the TWEAK/Fn14-related pathological outcomes in the aforementioned diseases and on the other hand, on the preclinical experience that have been made so far with TWEAK and Fn14 targeting drugs.
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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.