ArticleNature communications2017
Silencing Nfix rescues muscular dystrophy by delaying muscle regeneration.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Dynamic NFIX Promoter Usage Shapes Stem and Committed Myogenic States.International journal of molecular sciences · 2026Article
- Downstream Pathways of Dystrophin Deficiency in Duchenne Muscular Dystrophy: Implications for Muscle Degeneration and Regeneration.Journal of cachexia, sarcopenia and muscle · 2026Review
- Mechanistic Insights Into NFIX-Mediated DNA Recognition and Transcriptional Regulation in Skeletal Muscle.Smart medicine · 2026Article
- Structural basis of Nuclear Factor 1-X DNA recognition provides prototypic insight into the NFI family.Nature communications · 2025Article
- Intrinsic dysfunction in muscle stem cells lacking dystrophin begins during secondary myogenesis.Nature communications · 2025Article
- Intrinsic Muscle Stem Cell Dysfunction Contributes to Impaired Regeneration in the mdx Mouse.Journal of cachexia, sarcopenia and muscle · 2025Article
- Roles of the NFI/CTF gene family in transcription and development: update 2025.Academia biology · 2025Article
- Laminin-α2 chain deficiency in skeletal muscle causes dysregulation of multiple cellular mechanisms.Life science alliance · 2024Article
- Regulatory Role ofInternational journal of molecular sciences · 2024Article
- Macrophages in the Context of Muscle Regeneration and Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024Review
- MEK-inhibitors decrease Nfix in muscular dystrophy but induce unexpected calcifications, partially rescued with Cyanidin diet.iScience · 2024Article
- Significant phenotypic variability in a multigenerational family with anClinical case reports · 2024Article
- Molecular pathways involved in the control of contractile and metabolic properties of skeletal muscle fibers as potential therapeutic targets for Duchenne muscular dystrophy.Frontiers in physiology · 2024Review
- Regulation of Satellite Cells Functions during Skeletal Muscle Regeneration: A Critical Step in Physiological and Pathological Conditions.International journal of molecular sciences · 2023Review
- Expression of Myomaker and Myomerger in myofibers causes muscle pathology.Skeletal muscle · 2023Article
- Article
- Selective ablation of Nfix in macrophages attenuates muscular dystrophy by inhibiting fibro-adipogenic progenitor-dependent fibrosis.The Journal of pathology · 2022Article
- Depletion of skeletal muscle satellite cells attenuates pathology in muscular dystrophy.Nature communications · 2022Article
- The transcription factor NF-Y participates to stem cell fate decision and regeneration in adult skeletal muscle.Nature communications · 2021Article
- Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Muscular dystrophies are severe disorders due to mutations in structural genes, and are characterized by skeletal muscle wasting, compromised patient mobility, and respiratory functions. Although previous works suggested enhancing regeneration and muscle mass as therapeutic strategies, these led to no long-term benefits in humans. Mice lacking the transcription factor Nfix have delayed regeneration and a shift toward an oxidative fiber type. Here, we show that ablating or silencing the transcription factor Nfix ameliorates pathology in several forms of muscular dystrophy. Silencing Nfix in postnatal dystrophic mice, when the first signs of the disease already occurred, rescues the pathology and, conversely, Nfix overexpression in dystrophic muscles increases regeneration and markedly exacerbates the pathology. We therefore offer a proof of principle for a novel therapeutic approach for muscular dystrophies based on delaying muscle regeneration.
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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.