ArticleThe Journal of cell biology2006
Muscle aging is associated with compromised Ca2+ spark signaling and segregated intracellular Ca2+ release.
Article in The Journal of cell biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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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.
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Who cites it
75 citing papers in PubMed, 122 citations in OpenAlex.
- Reduced Synaptophysin-like 2 (MG29/SYPL2) Levels Mimic Age-Related Alterations in Skeletal Muscle Calcium Homeostasis and Lipid Signaling.Biomolecules · 2026Article
- STIM1 Reduction Prevents Tubular Aggregate Formation and Compromises Muscle Performance in Ageing Mice.Journal of cachexia, sarcopenia and muscle · 2025Article
- Branched-chain amino acids and L-alanine supplementation ameliorate calcium dyshomeostasis in sarcopenia: New insights for nutritional interventions.Frontiers in pharmacology · 2024Article
- Calcium's Role and Signaling in Aging Muscle, Cellular Senescence, and Mineral Interactions.International journal of molecular sciences · 2023Review
- Fiber-Type Shifting in Sarcopenia of Old Age: Proteomic Profiling of the Contractile Apparatus of Skeletal Muscles.International journal of molecular sciences · 2023Review
- Age-Related Dysfunction in Proteostasis and Cellular Quality Control in the Development of Sarcopenia.Cells · 2023Review
- Alteration of STIM1/Orai1-Mediated SOCE in Skeletal Muscle: Impact in Genetic Muscle Diseases and Beyond.Cells · 2021Review
- Altered CaMetabolites · 2021Review
- Profiling age-related muscle weakness and wasting: neuromuscular junction transmission as a driver of age-related physical decline.GeroScience · 2021Article
- MG53 suppresses interferon-β and inflammation via regulation of ryanodine receptor-mediated intracellular calcium signaling.Nature communications · 2020Article
- Multi-Staged Regulation of Lipid Signaling Mediators during Myogenesis by COX-1/2 Pathways.International journal of molecular sciences · 2019Article
- Dysregulated mitochondrial CaArchives of biochemistry and biophysics · 2019Review
- Cholesterol and the Safety Factor for Neuromuscular Transmission.International journal of molecular sciences · 2019Review
- Can Proprioceptive Training Reduce Muscle Fatigue in Patients With Motor Neuron Diseases? A New Direction of Treatment.Frontiers in physiology · 2019Review
- α-Motor neurons are spared from aging while their synaptic inputs degenerate in monkeys and mice.Aging cell · 2018Article
- Rejuvenation of the aged neuromuscular junction by exercise.Cell stress · 2018Review
- Role of miRNAs in skeletal muscle aging.Clinical interventions in aging · 2018Article
- A focus on extracellular CaExperimental & molecular medicine · 2017Review
- Molecular mechanisms and therapeutic interventions in sarcopenia.Osteoporosis and sarcopenia · 2017Review
- Targeted deletion ofFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Reduced homeostatic capacity for intracellular Ca2+ ([Ca2+]i) movement may underlie the progression of sarcopenia and contractile dysfunction during muscle aging. We report two alterations to Ca2+ homeostasis in skeletal muscle that are associated with aging. Ca2+ sparks, which are the elemental units of Ca2+ release from sarcoplasmic reticulum, are silent under resting conditions in young muscle, yet activate in a dynamic manner upon deformation of membrane structures. The dynamic nature of Ca2+ sparks appears to be lost in aged skeletal muscle. Using repetitive voltage stimulation on isolated muscle preparations, we identify a segregated [Ca2+]i reserve that uncouples from the normal excitation-contraction process in aged skeletal muscle. Similar phenotypes are observed in adolescent muscle null for a synaptophysin-family protein named mitsugumin-29 (MG29) that is involved in maintenance of muscle membrane ultrastructure and Ca2+ signaling. This finding, coupled with decreased expression of MG29 in aged skeletal muscle, suggests that MG29 expression is important in maintaining skeletal muscle Ca2+ homeostasis during aging.
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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.