ReviewJCI insight2023
Muscle: an independent contributor to the neuromuscular spinal muscular atrophy disease phenotype.
Review in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 16 citations in OpenAlex.
- Dynamic integration of skeletal muscle signals via extracellular vesicles in motor neuron diseases.Acta neuropathologica communications · 2026Review
- The evolving therapeutic landscape of spinal muscular atrophy - A scoping review of investigational agents, emerging delivery technologies and strategic innovations.British journal of clinical pharmacology · 2026Article
- Fibro-adipogenic progenitor cells from murine SMA muscles are intrinsically adipogenic.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- RNA biomarkers in spinal muscular atrophy: enhancing pathogenesis understanding and guiding precision medicine.Cellular and molecular life sciences : CMLS · 2026Review
- Collagen Scaffold Viscoelasticity Regulates Muscle Cell Phenotype.Advanced healthcare materials · 2026Article
- Cerebellar defects are a primary pathology in mouse models of spinal muscular atrophy.Brain pathology (Zurich, Switzerland) · 2025Article
- A qualitative, mixed-method approach to reaching consensus on function, fatigue, and fatigability outcomes in teens and adults living with spinal muscular atrophy.Orphanet journal of rare diseases · 2025Article
- Padua Days on Muscle and Mobility Medicine, March 25-29, 2025, Hotel Petrarca, Euganean Thermae, Italy: Program and Abstracts.European journal of translational myology · 2025Article
- SMN depletion impairs skeletal muscle formation and maturation in a mouse model of SMA.Human molecular genetics · 2025Article
- SMN Deficiency Induces an Early Non-Atrophic Myopathy with Alterations in the Contractile and Excitatory Coupling Machinery of Skeletal Myofibers in the SMN∆7 Mouse Model of Spinal Muscular Atrophy.International journal of molecular sciences · 2024Article
- Taldefgrobep Alfa and the Phase 3 RESILIENT Trial in Spinal Muscular Atrophy.International journal of molecular sciences · 2024Review
- Characterization of SMA type II skeletal muscle from treated patients shows OXPHOS deficiency and denervation.JCI insight · 2024Article
- Ubiquitination Insight from Spinal Muscular Atrophy-From Pathogenesis to Therapy: A Muscle Perspective.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Spinal muscular atrophy (SMA) is a pediatric-onset neuromuscular disorder caused by insufficient survival motor neuron (SMN) protein. SMN restorative therapies are now approved for the treatment of SMA; however, they are not curative, likely due to a combination of imperfect treatment timing, inadequate SMN augmentation, and failure to optimally target relevant organs. Here, we consider the implications of imperfect treatment administration, focusing specifically on outcomes for skeletal muscle. We examine the evidence that muscle plays a contributing role in driving neuromuscular dysfunction in SMA. Next, we discuss how SMN might regulate the health of myofibers and their progenitors. Finally, we speculate on therapeutic outcomes of failing to raise muscle SMN to healthful levels and present strategies to restore function to this tissue to ensure better treatment results.
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.