ArticleMolecular therapy : the journal of the American Society of Gene Therapy2020
miR-206 Reduces the Severity of Motor Neuron Degeneration in the Facial Nuclei of the Brainstem in a Mouse Model of SMA.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 34 citations in OpenAlex.
- The miR-206-3p/Cpeb1 axis delays acetylcholine receptor degradation and preserves neuromuscular junction stability in denervation-induced muscle atrophy.Cellular and molecular life sciences : CMLS · 2026Article
- MyomiR Networks in Spinal Muscular Atrophy: Associations With Clinical Severity and Treatment Response.Molecular neurobiology · 2026Article
- The amino acid transporter LAT1 coordinates proper motor function at the perinatal stage.Cell death & disease · 2026Article
- Novel Translational Concept: Axon-to-Muscle Exosomal Signaling as an Emerging Therapeutic Target in Spinal Muscular Atrophy.Biomedicines · 2025Review
- MiR-140-3p regulates axonal motor protein KIF5A and contributes to axonal transport degeneration in SMA.Cell death discovery · 2025Article
- Application of Biomarkers in Spinal Muscular Atrophy.International journal of molecular sciences · 2025Review
- Modulation of ZnT-1 by Let7a unveils a therapeutic potential in amyotrophic lateral sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Dysregulated balance of D- and L-amino acids modulating glutamatergic neurotransmission in severe spinal muscular atrophy.Neurobiology of disease · 2025Article
- Identifying Water-Salt Homeostasis and Inflammatory Response in Pathological Cardiac Surgery-Associated Acute Kidney Injury: NT-proBNP-related lncRNAs and miRNAs as Novel Diagnostic Biomarkers and Therapeutic Targets.International journal of medical sciences · 2025Article
- Neuronal innervation regulates the secretion of neurotrophic myokines and exosomes from skeletal muscle.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Diving into progress: a review on current therapeutic advancements in spinal muscular atrophy.Frontiers in neurology · 2024Review
- MicroRNAs as a Tool for Differential Diagnosis of Neuromuscular Disorders.Neuromolecular medicine · 2023Article
- SMN deficiency perturbs monoamine neurotransmitter metabolism in spinal muscular atrophy.Communications biology · 2023Article
- GKLOMLI: a link prediction model for inferring miRNA-lncRNA interactions by using Gaussian kernel-based method on network profile and linear optimization algorithm.BMC bioinformatics · 2023Article
- MiRNA-206 Affects the Recovery of Sciatic Function by Stimulating BDNF Activity through the Down-regulation of Notch3 Expression.Journal of musculoskeletal & neuronal interactions · 2023Article
- Autophagy in spinal muscular atrophy: from pathogenic mechanisms to therapeutic approaches.Frontiers in cellular neuroscience · 2023Review
- Emerging roles and mechanisms of miR-206 in human disorders: a comprehensive review.Cancer cell international · 2022Review
- Role of MicroRNAs, Aptamers in Neuroinflammation and Neurodegenerative Disorders.Cellular and molecular neurobiology · 2022Review
- Preconditioning in hypoxic-ischemic neonate mice triggers NaCell death discovery · 2022Article
- Response of plasma microRNAs to nusinersen treatment in patients with SMA.Annals of clinical and translational neurology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal muscular atrophy (SMA) is a severe neuromuscular disease affecting infants caused by alterations of the survival motor neuron gene, which results in progressive degeneration of motor neurons (MNs). Although an effective treatment for SMA patients has been recently developed, the molecular pathway involved in selective MN degeneration has not been yet elucidated. In particular, miR-206 has been demonstrated to play a relevant role in the regeneration of neuromuscular junction in several MN diseases, and particularly it is upregulated in the quadriceps, tibialis anterior, spinal cord, and serum of SMA mice. In the present paper, we demonstrated that miR-206 was transiently upregulated also in the brainstem of the mouse model of SMA, SMAΔ7, in the early phase of the disease paralleling MN degeneration and was down-regulated in the late symptomatic phase. To prevent this downregulation, we intracerebroventricularly injected miR-206 in SMA pups, demonstrating that miR-206 reduced the severity of SMA pathology, slowing down disease progression, increasing survival rate, and improving behavioral performance of mice. Interestingly, exogenous miRNA-206-induced upregulation caused a reduction of the predicted target sodium calcium exchanger isoform 2, NCX2, one of the main regulators of intracellular [Ca
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.