ArticleLife sciences2020
Fibroblast growth factor-inducible 14 mediates macrophage infiltration in heart to promote pressure overload-induced cardiac dysfunction.
Article in Life sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 33 citations in OpenAlex.
- Impaired adenosine pathways in HFpEF: insights into cardiorenal alterations and endothelial responses.Frontiers in pharmacology · 2026Article
- Circulating Extracellular Vesicles from Heart Failure Patients Inhibit Human Cardiomyocyte Activities.Journal of cardiovascular translational research · 2025Article
- Article
- The two-pore KAmerican journal of physiology. Heart and circulatory physiology · 2025Article
- Article
- TWEAK-Fn14: a promising target for cardio-cerebrovascular diseases and brain-heart syndrome.Frontiers in immunology · 2025Review
- Extracellular Vesicle-Associated TWEAK Contributes to Vascular Inflammation and Remodeling During Acute Cellular Rejection.JACC. Basic to translational science · 2023Article
- Exocyst inactivation in urothelial cells disrupts autophagy and activates non-canonical NF-κB signaling.Disease models & mechanisms · 2022Article
- Empagliflozin Disrupts a Tnfrsf12a-Mediated Feed Forward Loop That Promotes Left Ventricular Hypertrophy.Cardiovascular drugs and therapy · 2022Article
- Inhibition of TWEAK/Tnfrsf12a axis protects against acute liver failure by suppressing RIPK1-dependent apoptosis.Cell death discovery · 2022Article
- The TWEAK/Fn14/CD163 axis-implications for metabolic disease.Reviews in endocrine & metabolic disorders · 2022Review
- Analysis of myocardial cellular gene expression during pressure overload reveals matrix based functional intercellular communication.iScience · 2022Article
- The heart under pressure: immune cells in fibrotic remodeling.Current opinion in physiology · 2022Article
- Higher levels of TWEAK and matrix metalloproteinase-3 during the acute phase of myocardial infarction are associated with adverse left ventricular remodeling.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2021Article
- Triptolide improves myocardial fibrosis in rats through inhibition of nuclear factor kappa B and NLR family pyrin domain containing 3 inflammasome pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- The Cell Surface Receptors Ror1/2 Control Cardiac Myofibroblast Differentiation.Journal of the American Heart Association · 2021Article
- Adding insult to injury - Inflammation at the heart of cardiac fibrosis.Cellular signalling · 2021Review
- Maternal High Fat Diet and Diabetes Disrupts Transcriptomic Pathways That Regulate Cardiac Metabolism and Cell Fate in Newborn Rat Hearts.Frontiers in endocrinology · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
aimsHeart failure (HF) is characterized by compromised cardiac structure and function. Previous work has identified a link between upregulation of pro-inflammatory cytokines and HF. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a pro-inflammatory cytokine, which binds to fibroblast growth factor inducible 14 (Fn14), a ubiquitously expressed cell-surface receptor. The objective of this study was to investigate the role of TWEAK/Fn14 pathway in promoting cardiac inflammation under non ischemic stress conditions. MAIN
methodsWild type (WT) and Fn14 knock out (Fn14 KEY
findingsFn14 SIGNIFICANCE: Our findings support an important role for the TWEAK/Fn14 promoting macrophage infiltration and fibrosis in heart under non-ischemic stress, with potential for therapeutic intervention to improve cardiac function in the setting of HF.
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What OpenQuestion holds
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.