ArticleHuman molecular genetics2015
TWEAK/Fn14, a pathway and novel therapeutic target in myotonic dystrophy.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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Who cites it
26 citing papers in PubMed, 41 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
- Convergent innate immune and regulated cell-death pathways in selected myopathies.Frontiers in immunology · 2026Review
- Inhibition of TWEAK/Fn14 Ameliorates Sarcopenic Obesity by Restoring Mitochondrial Biogenesis via the AMPK/SIRT1/PGC-1α Axis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Multiple Defects in Muscle Regeneration in the HSALR Mouse Model of RNA Toxicity.International journal of molecular sciences · 2025Article
- Fn14 promotes myoblast fusion during regenerative myogenesis.Life science alliance · 2023Article
- From in vivo to in vitro: exploring the key molecular and cellular aspects of human female gametogenesis.Human cell · 2023Review
- 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
- Methotrexate Mechanism of Action in Plaque Psoriasis: Something New in the Old View.The Journal of clinical and aesthetic dermatology · 2022Article
- Modeling muscle regeneration in RNA toxicity mice.Human molecular genetics · 2021Article
- Targeted splice sequencing reveals RNA toxicity and therapeutic response in myotonic dystrophy.Nucleic acids research · 2021Article
- Neuromuscular Development and Disease: Learning FromFrontiers in cell and developmental biology · 2021Review
- Overlapping mechanisms of lncRNA and expanded microsatellite RNA.Wiley interdisciplinary reviews. RNA · 2021Review
- Brain Pathogenesis and Potential Therapeutic Strategies in Myotonic Dystrophy Type 1.Frontiers in aging neuroscience · 2021Review
- Molecular Profiling Reveals a Common Metabolic Signature of Tissue Fibrosis.Cell reports. Medicine · 2020Article
- Systemic therapy in an RNA toxicity mouse model with an antisense oligonucleotide therapy targeting a non-CUG sequence within the DMPK 3'UTR RNA.Human molecular genetics · 2020Article
- miR-7 Restores Phenotypes in Myotonic Dystrophy Muscle Cells by Repressing Hyperactivated Autophagy.Molecular therapy. Nucleic acids · 2020Article
- MBNL1 overexpression is not sufficient to rescue the phenotypes in a mouse model of RNA toxicity.Human molecular genetics · 2019Article
- Myotonic Dystrophies: Targeting Therapies for Multisystem Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- Pharmacological and physiological activation of AMPK improves the spliceopathy in DM1 mouse muscles.Human molecular genetics · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Myotonic dystrophy type 1 (DM1), the most prevalent muscular dystrophy in adults, is characterized by progressive muscle wasting and multi-systemic complications. DM1 is the prototype for disorders caused by RNA toxicity. Currently, no therapies exist. Here, we identify that fibroblast growth factor-inducible 14 (Fn14), a member of the tumor necrosis factor receptor super-family, is induced in skeletal muscles and hearts of mouse models of RNA toxicity and in tissues from DM1 patients, and that its expression correlates with severity of muscle pathology. This is associated with downstream signaling through the NF-κB pathways. In mice with RNA toxicity, genetic deletion of Fn14 results in reduced muscle pathology and better function. Importantly, blocking TWEAK/Fn14 signaling with an anti-TWEAK antibody likewise improves muscle histopathology and functional outcomes in affected mice. These results reveal new avenues for therapeutic development and provide proof of concept for a novel therapeutic target for which clinically available therapy exists to potentially treat muscular dystrophy in DM1.
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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.