ReviewFrontiers in immunology2014
TWEAK-Fn14 Cytokine-Receptor Axis: A New Player of Myocardial Remodeling and Cardiac Failure.
Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Genetic Evidence Linking Inflammatory Cytokines and Blood Metabolites to Heart Failure Risk.Cardiovascular therapeutics · 2026Article
- Interplay of rheumatoid arthritis and cardiovascular disease: Insights and prospects.SAGE open medicine · 2025Review
- TWEAK-Fn14: a promising target for cardio-cerebrovascular diseases and brain-heart syndrome.Frontiers in immunology · 2025Review
- Sodium-glucose Cotransporter 2 Inhibitors and Pathological Myocardial Hypertrophy.Current drug targets · 2023Article
- Empagliflozin Disrupts a Tnfrsf12a-Mediated Feed Forward Loop That Promotes Left Ventricular Hypertrophy.Cardiovascular drugs and therapy · 2022Article
- Therapeutic efficacy and safety of a human fusion construct targeting the TWEAK receptor Fn14 and containing a modified granzyme B.Journal for immunotherapy of cancer · 2020Article
- Review
- TRAF3IP2 mediates TWEAK/TWEAKR-induced pro-fibrotic responses in cultured cardiac fibroblasts and the heart.Journal of molecular and cellular cardiology · 2018Article
- Effect of influenza vaccine on tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in older adults.Vaccine · 2018Article
- Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice.Journal of immunology research · 2018Article
- Article
- Inflammatory Mediators Drive Adverse Right Ventricular Remodeling and Dysfunction and Serve as Potential Biomarkers.Frontiers in physiology · 2018Review
- Silent disease progression in clinically stable heart failure.European journal of heart failure · 2017Review
- Beyond TNF: TNF superfamily cytokines as targets for the treatment of rheumatic diseases.Nature reviews. Rheumatology · 2017Review
- TWEAK/Fn14 Activation Participates in Skin Inflammation.Mediators of inflammation · 2017Review
- Serum Levels of TNF Receptor Ligands Are Dysregulated in Sepsis and Predict Mortality in Critically Ill Patients.PloS one · 2016Article
- TWEAK protects cardiomyocyte against apoptosis in a PI3K/AKT pathway dependent manner.American journal of translational research · 2016Article
- Article
- Association between miR-181b and PKG 1 in myocardial hypertrophy and its clinical implications.Experimental and therapeutic medicine · 2015Article
- Fn14, a Downstream Target of the TGF-β Signaling Pathway, Regulates Fibroblast Activation.PloS one · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor (TNF) has been firmly established as a pathogenic factor in heart failure, a significant socio-economic burden. In this review, we will explore the role of other members of the TNF/TNF receptor superfamily (TNFSF/TNFRSF) in cardiovascular diseases (CVDs) focusing on TWEAK and its receptor Fn14, new players in myocardial remodeling and heart failure. The TWEAK/Fn14 pathway controls a variety of cellular activities such as proliferation, differentiation, and apoptosis and has diverse biological functions in pathological mechanisms like inflammation and fibrosis that are associated with CVDs. Furthermore, it has recently been shown that the TWEAK/Fn14 axis is a positive regulator of cardiac hypertrophy and that deletion of Fn14 receptor protects from right heart fibrosis and dysfunction. We discuss the potential use of the TWEAK/Fn14 axis as biomarker for CVDs as well as therapeutic target for future treatment of human heart failure based on supporting data from animal models and in vitro studies. Collectively, existing data strongly suggest the TWEAK/Fn14 axis as a potential new therapeutic target for achieving cardiac protection in patients with CVDs.
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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.