ArticlePflugers Archiv : European journal of physiology2010
Altered myoplasmic Ca(2+) handling in rat fast-twitch skeletal muscle fibres during disuse atrophy.
Article in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Mitochondrial fusion is frequent in skeletal muscle and supports excitation-contraction coupling.The Journal of cell biology · 2014Trial
- A controversial issue: Can mitochondria modulate cytosolic calcium and contraction of skeletal muscle fibers?The Journal of general physiology · 2022Review
- Short-term step reduction reduces citrate synthase activity without altering skeletal muscle markers of oxidative metabolism or insulin-mediated signaling in young males.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Comprehensive Simulation of CaInternational journal of molecular sciences · 2021Article
- Altered CaMetabolites · 2021Review
- Translational research on Myology and Mobility Medicine: 2021 semi-virtual PDM3 from Thermae of Euganean Hills, May 26 - 29, 2021.European journal of translational myology · 2021Article
- Mitochondrial health and muscle plasticity after spinal cord injury.European journal of applied physiology · 2019Review
- SPEG-deficient skeletal muscles exhibit abnormal triad and defective calcium handling.Human molecular genetics · 2018Article
- Impaired Ca(2+) release contributes to muscle weakness in a rat model of critical illness myopathy.Critical care (London, England) · 2016Article
- CUG-BP1 regulates RyR1 ASI alternative splicing in skeletal muscle atrophy.Scientific reports · 2015Article
- Reconsidering the Role of Mitochondria in Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2015Review
- Altered Ca(2+) signaling in skeletal muscle fibers of the R6/2 mouse, a model of Huntington's disease.The Journal of general physiology · 2014Article
- The stress protein/chaperone Grp94 counteracts muscle disuse atrophy by stabilizing subsarcolemmal neuronal nitric oxide synthase.Antioxidants & redox signaling · 2014Article
- Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy.Biological chemistry · 2013Review
- Mitochondrial signaling contributes to disuse muscle atrophy.American journal of physiology. Endocrinology and metabolism · 2012Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium-dependent signalling pathways are believed to play an important role in skeletal muscle atrophy, but whether intracellular Ca(2+) homeostasis is affected in that situation remains obscure. We show here that there is a 20% atrophy of the fast-type flexor digitorum brevis (FDB) muscle in rats hind limb unloaded (HU) for 2 weeks, with no change in fibre type distribution. In voltage-clamp experiments, the amplitude of the slow Ca(2+) current was found similar in fibres from control and HU animals. In fibres loaded with the Ca(2+) dye indo-1, the value for the rate of [Ca(2+)] decay after the end of 5-100-ms-long voltage-clamp depolarisations from -80 to +10 mV was found to be 30-50% lower in fibres from HU animals. This effect was consistent with a reduced contribution of both saturable and non-saturable components of myoplasmic Ca(2+) removal. However, there was no change in the relative amount of parvalbumin, and type 1 sarco-endoplasmic reticulum Ca(2+)-ATPase was increased by a factor of three in the atrophied muscles. Confocal imaging of mitochondrial membrane potential showed that atrophied FDB fibres had significantly depolarized mitochondria as compared to control fibres. Depolarization of mitochondria in control fibres with carbonyl cyanide-p-trifluoromethoxyphenylhydrazone induced a slowing of the decay of [Ca(2+)] transients accompanied by an increase in resting [Ca(2+)] and a reduction of the peak amplitude of the transients. Overall results provide the first functional evidence for severely altered intracellular Ca(2+) removal capabilities in atrophied fast-type muscle fibres and highlight the possible contribution of reduced mitochondrial polarisation.
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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.