ReviewMolecular biology reports2012
The role of TWEAK/Fn14 in cardiac remodeling.
Review in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
11 citing papers in PubMed.
- Chronic intermittent electronic cigarette exposure induces cardiac dysfunction and atherosclerosis in apolipoprotein-E knockout mice.American journal of physiology. Heart and circulatory physiology · 2019Article
- TRAF3IP2 mediates TWEAK/TWEAKR-induced pro-fibrotic responses in cultured cardiac fibroblasts and the heart.Journal of molecular and cellular cardiology · 2018Article
- Article
- Pay attention to cardiac remodeling in cancer cachexia.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2016Review
- TWEAK protects cardiomyocyte against apoptosis in a PI3K/AKT pathway dependent manner.American journal of translational research · 2016Article
- Article
- TWEAK/Fn14, a pathway and novel therapeutic target in myotonic dystrophy.Human molecular genetics · 2015Article
- Autophagy is a regulator of TGF-β1-induced fibrogenesis in primary human atrial myofibroblasts.Cell death & disease · 2015Article
- Article
- New and emerging biomarkers in left ventricular systolic dysfunction--insight into dilated cardiomyopathy.Journal of cardiovascular translational research · 2013Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathophysiological basis of heart failure is cardiac remodeling, a process that comprises structural and functional changes including cardiomyocyte proliferation, hypertrophy, necrosis, apoptosis, autophagy, interstitial fibrosis, contractile dysfunction and ventricular dilatation. Accumulating evidence demonstrate that tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is involved in the process by binding its receptor fibroblast growth factor-inducible molecule 14 (Fn14). In this review, we will discuss the potential role of the TWEAK/Fn14 axis in cardiac remodeling, elucidate its possible mechanisms and explore new therapeutic targets for heart failure.
Indexed as
Identifiers
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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.