ArticleCell stress2017
Targeting Nfix to fix muscular dystrophies.
Article in Cell stress, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Comparative Transcriptomic Profiling in Patients Affected by Duchenne and Becker Muscular Dystrophies: A Focus on ECM Genes Dysregulation.International journal of molecular sciences · 2025Article
- NFIX suppresses breast cancer cell proliferation by delaying mitosis through downregulation of CDK1 expression.Cell death discovery · 2025Article
- Roles of the NFI/CTF gene family in transcription and development: update 2025.Academia biology · 2025Article
- NFIXing Cancer: The Role of NFIX in Oxidative Stress Response and Cell Fate.International journal of molecular sciences · 2023Review
- Oxidative Stress, Inflammation and Connexin Hemichannels in Muscular Dystrophies.Biomedicines · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Muscular dystrophies (MDs) are still incurable heterogeneous diseases, characterized by muscle wasting, replacement by fibrotic tissue, and increasing weakness, which in severe cases, such as Duchenne MD, lead to premature death. MDs are due to mutations encompassing different dystrophin-glycoprotein complex (DGC) genes, which code for structural proteins that anchor the cytoskeleton to the extracellular matrix, thus conferring myofiber stability. All mutations destabilizing this complex result in different MD forms, with varying levels of severity. Independently of the genetic defect, MDs share common hallmarks, characterized by continuous cycles of muscle degeneration, due to lack of structural support during contraction, followed by regeneration cycles by satellite cells (SCs), the canonical myogenic stem cells of adult muscle. However, dystrophic SCs generate new fibres which are also prone to degeneration so that, after many cycles of degeneration/regeneration, this cell population is exhausted and muscle is replaced by connective and adipose tissue. At this stage, any therapeutic intervention is likely to fail.
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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.