ArticleCell death & disease2013
Lithium chloride attenuates cell death in oculopharyngeal muscular dystrophy by perturbing Wnt/β-catenin pathway.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- β-Catenin is central to DUX4-driven network rewiring in facioscapulohumeral muscular dystrophy.Journal of the Royal Society, Interface · 2015Pooled it
- Elf3 drives β-catenin transactivation and associates with poor prognosis in colorectal cancer.Cell death & disease · 2014Trial
- Age Is Just a Number: Progress and Obstacles in the Discovery of New Candidate Drugs for Sarcopenia.Cells · 2023Review
- Phloretin induces G2/M arrest and apoptosis by suppressing the β-catenin signaling pathway in colorectal carcinoma cells.Apoptosis : an international journal on programmed cell death · 2023Article
- Lithium in Cancer Therapy: Friend or Foe?Cancers · 2023Review
- DVL1 and DVL3 require nuclear localisation to regulate proliferation in human myoblasts.Scientific reports · 2022Article
- Lithium causes differential effects on postsynaptic stability in normal and denervated neuromuscular synapses.Scientific reports · 2021Article
- Allosteric Modulation of GSK-3β as a New Therapeutic Approach in Limb Girdle Muscular Dystrophy R1 Calpain 3-Related.International journal of molecular sciences · 2021Article
- Lithium Chloride Protects against Sepsis-Induced Skeletal Muscle Atrophy and Cancer Cachexia.Cells · 2021Article
- Drug Repurposing for Targeting Acute Leukemia WithFrontiers in pharmacology · 2021Review
- Article
- Impaired Regeneration in Dystrophic Muscle-New Target for Therapy.Frontiers in molecular neuroscience · 2020Article
- RNA-Based Therapy Utilizing Oculopharyngeal Muscular Dystrophy Transcript Knockdown and Replacement.Molecular therapy. Nucleic acids · 2019Article
- Application of the parametric bootstrap for gene-set analysis of gene-environment interactions.European journal of human genetics : EJHG · 2018Article
- Valproic acid is protective in cellular and worm models of oculopharyngeal muscular dystrophy.Neurology · 2018Article
- Scar management in burn injuries using drug delivery and molecular signaling: Current treatments and future directions.Advanced drug delivery reviews · 2018Review
- Apigenin-induced lysosomal degradation of β-catenin in Wnt/β-catenin signaling.Scientific reports · 2017Article
- Activation of the wnt/β-Catenin Signaling Pathway in Polymyositis, Dermatomyositis and Duchenne Muscular Dystrophy.Journal of clinical neurology (Seoul, Korea) · 2016Article
- Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation.Cell discovery · 2016Article
- MuSK frizzled-like domain is critical for mammalian neuromuscular junction formation and maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Expansion of polyalanine tracts causes at least nine inherited human diseases. Among these, a polyalanine tract expansion in the poly (A)-binding protein nuclear 1 (expPABPN1) causes oculopharyngeal muscular dystrophy (OPMD). So far, there is no treatment for OPMD patients. Developing drugs that efficiently sustain muscle protection by activating key cell survival mechanisms is a major challenge in OPMD research. Proteins that belong to the Wnt family are known for their role in both human development and adult tissue homeostasis. A hallmark of the Wnt signaling pathway is the increased expression of its central effector, beta-catenin (β-catenin) by inhibiting one of its upstream effector, glycogen synthase kinase (GSK)3β. Here, we explored a pharmacological manipulation of a Wnt signaling pathway using lithium chloride (LiCl), a GSK-3β inhibitor, and observed the enhanced expression of β-catenin protein as well as the decreased cell death normally observed in an OPMD cell model of murine myoblast (C2C12) expressing the expanded and pathogenic form of the expPABPN1. Furthermore, this effect was also observed in primary cultures of mouse myoblasts expressing expPABPN1. A similar effect on β-catenin was also observed when lymphoblastoid cells lines (LCLs) derived from OPMD patients were treated with LiCl. We believe manipulation of the Wnt/β-catenin signaling pathway may represent an effective route for the development of future therapy for patients with OPMD.
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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.