ReviewCellular and molecular life sciences : CMLS2016
Polyglutamine androgen receptor-mediated neuromuscular disease.
Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 31 citations in OpenAlex.
- Androgen signaling is dispensable for fetal testis formation: decoupling testis organogenesis from fetal masculinization programming.Molecular human reproduction · 2026Review
- Restoring early postnatal synaptic dysregulation rescues motor neuron degeneration in a mouse model of Spinal and Bulbar Muscular Atrophy.Nature communications · 2026Article
- PROTACs therapeutically target the polyglutamine androgen receptor in spinal and bulbar muscular atrophy models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Reviewing the Structure-Function Paradigm in Polyglutamine Disorders: A Synergistic Perspective on Theoretical and Experimental Approaches.International journal of molecular sciences · 2024Review
- Exercise attenuates polyglutamine-mediated neuromuscular degeneration in a mouse model of spinal and bulbar muscular atrophy.Journal of cachexia, sarcopenia and muscle · 2024Article
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Review
- Deubiquitinase USP7 contributes to the pathogenicity of spinal and bulbar muscular atrophy.The Journal of clinical investigation · 2021Article
- The Impact of Mitochondrial Deficiencies in Neuromuscular Diseases.Antioxidants (Basel, Switzerland) · 2020Review
- Role of Mutant TBP in Regulation of Myogenesis on Muscle Satellite Cells.Current medical science · 2019Article
- Genetic approaches to the treatment of inherited neuromuscular diseases.Human molecular genetics · 2019Review
- DNA methylation inhibitor attenuates polyglutamine-induced neurodegeneration by regulating Hes5.EMBO molecular medicine · 2019Article
- Polyglutamine Repeats in Neurodegenerative Diseases.Annual review of pathology · 2019Review
- Expression of Human Endogenous Retrovirus-K in Spinal and Bulbar Muscular Atrophy.Frontiers in neurology · 2019Article
- Autophagic and Proteasomal Mediated Removal of Mutant Androgen Receptor in Muscle Models of Spinal and Bulbar Muscular Atrophy.Frontiers in endocrinology · 2019Article
- Systemic Delivery of MicroRNA Using Recombinant Adeno-associated Virus Serotype 9 to Treat Neuromuscular Diseases in Rodents.Journal of visualized experiments : JoVE · 2018Article
- Androgen receptor polyglutamine expansion drives age-dependent quality control defects and muscle dysfunction.The Journal of clinical investigation · 2018Article
- Intrinsic Disorder in Proteins with Pathogenic Repeat Expansions.Molecules (Basel, Switzerland) · 2017Review
- Correlation of insulin resistance and motor function in spinal and bulbar muscular atrophy.Journal of neurology · 2017Article
- Network analysis reveals crosstalk between autophagy genes and disease genes.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
An expanded polyglutamine (polyQ) tract at the amino-terminus of the androgen receptor (AR) confers toxic properties responsible for neuronal and non-neuronal degeneration in spinal and bulbar muscular atrophy (SBMA), one of nine polyQ expansion diseases. Both lower motor neurons and peripheral tissues, including skeletal muscle, are affected, supporting the notion that SBMA is not a pure motor neuron disease but a degenerative disorder of the neuromuscular system. Here, we review experimental evidence demonstrating both nerve and muscle degeneration in SBMA model systems and patients. We propose that polyQ AR toxicity targets these components in a time-dependent fashion, with muscle pathology predominating early and motor neuron loss becoming more significant at late stages. This model of pathogenesis has important therapeutic implications, suggesting that symptoms arising from degeneration of nerve or muscle predominate at different points and that directed interventions targeting these components will be variably effective depending upon disease progression.
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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.