ArticleExperimental gerontology2009
Role of Ca2+, membrane excitability, and Ca2+ stores in failing muscle contraction with aging.
Article in Experimental gerontology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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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.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Skeletal muscle transcriptomics identifies common pathways in nerve crush injury and ageing.Skeletal muscle · 2022Article
- STIM and Orai Mediated Regulation of Calcium Signaling in Age-Related Diseases.Frontiers in aging · 2022Review
- Altered CaMetabolites · 2021Review
- Improper Remodeling of Organelles Deputed to CaInternational journal of molecular sciences · 2021Review
- Dysregulated mitochondrial CaArchives of biochemistry and biophysics · 2019Review
- ORAI1 channel gating and selectivity is differentially altered by natural mutations in the first or third transmembrane domain.The Journal of physiology · 2019Article
- Role of STIM1/ORAI1-mediated store-operated CaCell calcium · 2018Review
- Skeletal muscle performance and ageing.Journal of cachexia, sarcopenia and muscle · 2018Review
- Rejuvenation of the aged neuromuscular junction by exercise.Cell stress · 2018Review
- SOCE Is Important for Maintaining Sarcoplasmic Calcium Content and Release in Skeletal Muscle Fibers.Biophysical journal · 2017Article
- Exercise-dependent formation of new junctions that promote STIM1-Orai1 assembly in skeletal muscle.Scientific reports · 2017Article
- Absence of physiological CaSkeletal muscle · 2017Article
- Parvalbumin gene transfer impairs skeletal muscle contractility in old mice.Human gene therapy · 2012Article
- Evolving concepts on the age-related changes in "muscle quality".Journal of cachexia, sarcopenia and muscle · 2012Article
- Expression and regulation of excitation-contraction coupling proteins in aging skeletal muscle.Current aging science · 2011Review
- Age-related changes in motor cortical properties and voluntary activation of skeletal muscle.Current aging science · 2011Review
- Posttetanic potentiation in mdx muscle.Journal of muscle research and cell motility · 2010Article
- Age- and gender-related changes in contractile properties of non-atrophied EDL muscle.PloS one · 2010Article
- Sarcoplasmic reticulum Ca2+ depletion in adult skeletal muscle fibres measured with the biosensor D1ER.Pflugers Archiv : European journal of physiology · 2010Article
- Hyperactive intracellular calcium signaling associated with localized mitochondrial defects in skeletal muscle of an animal model of amyotrophic lateral sclerosis.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Excitation-contraction (EC) coupling in a population of skeletal muscle fibers of aged mice becomes dependent on the presence of external Ca(2+) ions (Payne, A.M., Zheng, Z., Gonzalez, E., Wang, Z.M., Messi, M.L., Delbono, O., 2004b. External Ca(2+)-dependent excitation - contraction coupling in a population of aging mouse skeletal muscle fibers. J. Physiol. 560, 137-155.). However, the mechanism(s) underlying this process remain unknown. In this work, we examined the role of (1) extracellular Ca(2+); (2) voltage-induced influx of external Ca(2+) ions; (3) sarcoplasmic reticulum (SR) Ca(2+) depletion during repeated contractions; (4) store-operated Ca(2+) entry (SOCE); (5) SR ultrastructure; (6) SR subdomain localization of the ryanodine receptor; and (7) sarcolemmal excitability in muscle force decline with aging. These experiments show that external Ca(2+), but not Ca(2+) influx, is needed to maintain force upon repetitive fiber electrical stimulation. Decline in fiber force is associated with depressed SR Ca(2+) release. SR Ca(2+) depletion, SOCE, and the putative segregated Ca(2+) release store do not play a significant role in external Ca(2+)-dependent contraction. More importantly, a significant number of action potentials fail in senescent mouse muscle fibers subjected to a stimulation frequency. These results indicate that failure to generate action potentials accounts for decreased intracellular Ca(2+) mobilization and tetanic force in aging muscle exposed to a Ca(2+)-free medium.
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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.