ArticlePloS one2016
TWEAK Regulates Muscle Functions in a Mouse Model of RNA Toxicity.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 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
10 citing papers in PubMed, 11 citations in OpenAlex.
- TWEAK-induced alternative NF-κB signaling regulates Cxcl10 and Mymx to promote myoblast-to-myotube fusion and muscle regeneration.Communications biology · 2026Article
- Disruptions of cell signaling pathways in myotonic dystrophy type 1 skeletal muscle, their pathogenic impact, and potential for combinatorial therapeutics.The Journal of biological chemistry · 2026Review
- Multiple Defects in Muscle Regeneration in the HSALR Mouse Model of RNA Toxicity.International journal of molecular sciences · 2025Article
- Studying the Effect of MBNL1 and MBNL2 Loss in Skeletal Muscle Regeneration.International journal of molecular sciences · 2024Article
- Fn14 promotes myoblast fusion during regenerative myogenesis.Life science alliance · 2023Article
- Targeted ablation of Fn14 receptor improves exercise capacity and inhibits neurogenic muscle atrophy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Modeling muscle regeneration in RNA toxicity mice.Human molecular genetics · 2021Article
- Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy.The Journal of experimental medicine · 2021Article
- Controversies in TWEAK-Fn14 signaling in skeletal muscle atrophy and regeneration.Cellular and molecular life sciences : CMLS · 2020Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Myotonic dystrophy type 1 (DM1), the most common form of muscular dystrophy in adults, is caused by toxic RNAs produced from the mutant DM protein kinase (DMPK) gene. DM1 is characterized by progressive muscle wasting and weakness. Therapeutic strategies have mainly focused on targeting the toxic RNA. Previously, we found that fibroblast growth factor-inducible 14 (Fn14), the receptor for TWEAK, is induced in skeletal muscles and hearts of mouse models of RNA toxicity and that blocking TWEAK/Fn14 signaling improves muscle function and histology. Here, we studied the effect of Tweak deficiency in a RNA toxicity mouse model. The genetic deletion of Tweak in these mice significantly reduced muscle damage and improved muscle function. In contrast, administration of TWEAK in the RNA toxicity mice impaired functional outcomes and worsened muscle histopathology. These studies show that signaling via TWEAK is deleterious to muscle in RNA toxicity and support the demonstrated utility of anti-TWEAK therapeutics.
Indexed as
Identifiers
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.