ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2011
Upregulation of the CaV 1.1-ryanodine receptor complex in a rat model of critical illness myopathy.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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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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
12 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Mitochondrial Dysfunction in Intensive Care Unit-Acquired Weakness and Critical Illness Myopathy: A Narrative Review.International journal of molecular sciences · 2023Review
- A Temporal Examination of Cytoplasmic CaFrontiers in physiology · 2020Article
- Electrical Stimulation Prevents Preferential Skeletal Muscle Myosin Loss in Steroid-Denervation Rats.Frontiers in physiology · 2018Article
- Mechanism of ICU-acquired weakness: muscle contractility in critical illness.Intensive care medicine · 2017Article
- Impaired Ca(2+) release contributes to muscle weakness in a rat model of critical illness myopathy.Critical care (London, England) · 2016Article
- A conceptual framework: the early and late phases of skeletal muscle dysfunction in the acute respiratory distress syndrome.Critical care (London, England) · 2015Review
- The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill.Physiological reviews · 2015Review
- Distinct muscle apoptotic pathways are activated in muscles with different fiber types in a rat model of critical illness myopathy.Journal of muscle research and cell motility · 2015Article
- De novo expression of connexin hemichannels in denervated fast skeletal muscles leads to atrophy.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Functional classification of skeletal muscle networks. II. Applications to pathophysiology.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- Altered sodium channel-protein associations in critical illness myopathy.Skeletal muscle · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The processes that trigger severe muscle atrophy and loss of myosin in critical illness myopathy (CIM) are poorly understood. It has been reported that muscle disuse alters Ca(2+) handling by the sarcoplasmic reticulum. Since inactivity is an important contributor to CIM, this finding raises the possibility that elevated levels of the proteins involved in Ca(2+) handling might contribute to development of CIM. CIM was induced in 3- to 5-mo-old rats by sciatic nerve lesion and infusion of dexamethasone for 1 wk. Western blot analysis revealed increased levels of ryanodine receptor (RYR) isoforms-1 and -2 as well as the dihydropyridine receptor/voltage-gated calcium channel type 1.1 (DHPR/Ca(V) 1.1). Immunostaining revealed a subset of fibers with elevation of RYR1 and Ca(V) 1.1 that had severe atrophy and disorganization of sarcomeres. These findings suggest increased Ca(2+) release from the sarcoplasmic reticulum may be an important contributor to development of CIM. To assess the endogenous functional effects of increased intracellular Ca(2+) in CIM, proteolysis of α-fodrin, a well-known target substrate of Ca(2+)-activated proteases, was measured and found to be 50% greater in CIM. There was also selective degradation of myosin heavy chain relative to actin in CIM muscle. Taken together, our findings suggest that increased Ca(2+) release from the sarcoplasmic reticulum may contribute to pathology in CIM.
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Registered trials
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