ArticleProceedings of the National Academy of Sciences of the United States of America2000
Elevated subsarcolemmal Ca2+ in mdx mouse skeletal muscle fibers detected with Ca2+-activated K+ channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.
- Calcium antagonists for Duchenne muscular dystrophy.The Cochrane database of systematic reviews · 2008Pooled it
- Pharmacological Treatments and Therapeutic Targets in Muscle Dystrophies Generated by Alterations in Dystrophin-Associated Proteins.Medicina (Kaunas, Lithuania) · 2024Review
- A mechano- and heat-gated two-pore domain KProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Sarcoplasmic Reticulum CaCells · 2023Review
- Ion Channels of the Sarcolemma and Intracellular Organelles in Duchenne Muscular Dystrophy: A Role in the Dysregulation of Ion Homeostasis and a Possible Target for Therapy.International journal of molecular sciences · 2023Review
- P2 Receptor Signaling in Motor Units in Muscular Dystrophy.International journal of molecular sciences · 2023Review
- Postdevelopmental knockout of Orai1 improves muscle pathology in a mouse model of Duchenne muscular dystrophy.The Journal of general physiology · 2022Article
- Shared and distinct mechanisms of skeletal muscle atrophy: A narrative review.Ageing research reviews · 2021Review
- Alteration of STIM1/Orai1-Mediated SOCE in Skeletal Muscle: Impact in Genetic Muscle Diseases and Beyond.Cells · 2021Review
- Targeting Nrf2 for the treatment of Duchenne Muscular Dystrophy.Redox biology · 2021Review
- TRPCs: Influential Mediators in Skeletal Muscle.Cells · 2020Review
- GsMTx4-D provides protection to the D2.mdx mouse.Neuromuscular disorders : NMD · 2018Article
- Novel inhibitor candidates of TRPV2 prevent damage of dystrophic myocytes and ameliorate against dilated cardiomyopathy in a hamster model.Oncotarget · 2018Article
- Dystrophin gene expression and intracellular calcium changes in the giant freshwater prawn,Heliyon · 2017Article
- Mitochondrial Ca(2+) uptake in skeletal muscle health and disease.Science China. Life sciences · 2016Review
- Cancer cachexia causes skeletal muscle damage via transient receptor potential vanilloid 2-independent mechanisms, unlike muscular dystrophy.Journal of cachexia, sarcopenia and muscle · 2016Article
- Article
- Comparative Label-Free Mass Spectrometric Analysis of Mildly versus Severely Affected mdx Mouse Skeletal Muscles Identifies Annexin, Lamin, and Vimentin as Universal Dystrophic Markers.Molecules (Basel, Switzerland) · 2015Article
- Primary Murine Myotubes as a Model for Investigating Muscular Dystrophy.BioMed research international · 2015Article
- Na+ dysregulation coupled with Ca2+ entry through NCX1 promotes muscular dystrophy in mice.Molecular and cellular biology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy results from the lack of dystrophin, a cytoskeletal protein associated with the inner surface membrane, in skeletal muscle. The cellular mechanisms responsible for the progressive skeletal muscle degeneration that characterizes the disease are still debated. One hypothesis suggests that the resting sarcolemmal permeability for Ca(2+) is increased in dystrophic muscle, leading to Ca(2+) accumulation in the cytosol and eventually to protein degradation. However, more recently, this hypothesis was challenged seriously by several groups that did not find any significant increase in the global intracellular Ca(2+) in muscle from mdx mice, an animal model of the human disease. In the present study, using plasma membrane Ca(2+)-activated K(+) channels as subsarcolemmal Ca(2+) probe, we tested the possibility of a Ca(2+) accumulation at the restricted subsarcolemmal level in mdx skeletal muscle fibers. Using the cell-attached configuration of the patch-clamp technique, we demonstrated that the voltage threshold for activation of high conductance Ca(2+)-activated K(+) channels is significantly lower in mdx than in control muscle, suggesting a higher subsarcolemmal [Ca(2+)]. In inside-out patches, we showed that this shift in the voltage threshold for high conductance Ca(2+)-activated K(+) channel activation could correspond to a approximately 3-fold increase in the subsarcolemmal Ca(2+) concentration in mdx muscle. These data favor the hypothesis according to which an increased calcium entry is associated with the absence of dystrophin in mdx skeletal muscle, leading to Ca(2+) overload at the subsarcolemmal level.
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