ReviewJournal of muscle research and cell motility2006
Dysregulation of sodium channel gating in critical illness myopathy.
Review in Journal of muscle research and cell motility, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Clinical review: Critical illness polyneuropathy and myopathy.Critical care (London, England) · 2008Pooled it
- Critical Illness Myopathy: Diagnostic Approach and Resulting Therapeutic Implications.Current treatment options in neurology · 2022Review
- New Challenges Resulting From the Loss of Function of NaFrontiers in pharmacology · 2021Review
- Prognostic value of NT-proBNP levels in the acute phase of sepsis on lower long-term physical function and muscle strength in sepsis survivors.Critical care (London, England) · 2019Article
- Clinical review: peripheral muscular ultrasound in the ICU.Annals of intensive care · 2019Review
- Impaired Ca(2+) release contributes to muscle weakness in a rat model of critical illness myopathy.Critical care (London, England) · 2016Article
- Muscle regeneration after sepsis.Critical care (London, England) · 2016Article
- The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill.Physiological reviews · 2015Review
- [Intensive care unit-acquired weakness in the critically ill : critical illness polyneuropathy and critical illness myopathy].Der Anaesthesist · 2011Review
- Have we found the prevention for intensive care unit-acquired paresis?Critical care (London, England) · 2010Article
- Noninvasive model of sciatic nerve conduction in healthy and septic mice: reliability and normative data.Muscle & nerve · 2009Article
- Sepsis-induced myopathy.Critical care medicine · 2009Review
- Critical illness polyneuropathy and myopathy in the intensive care unit.Nature reviews. Neurology · 2009Review
- Inactivation of sodium channels underlies reversible neuropathy during critical illness in rats.The Journal of clinical investigation · 2009Article
- Treatment of neuromuscular channelopathies: current concepts and future prospects.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2008Review
- Mechanisms of neuromuscular dysfunction in critical illness.Critical care clinics · 2008Review
- Nav channel mechanosensitivity: activation and inactivation accelerate reversibly with stretch.Biophysical journal · 2007Article
- Diagnosis and management of critical illness polyneuropathy and critical illness myopathy.Current treatment options in neurology · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Critical illness myopathy (CIM) is the most common caused of acquired weakness in critically ill patients. While atrophy of muscle fibers causes weakness, the primary cause of acute weakness is loss of muscle excitability. Studies in an animal model of CIM suggest that both depolarization of the resting potential and a hyperpolarized shift in the voltage dependence of sodium channel gating combine to cause inexcitability. In active adult skeletal muscle the only sodium channel isoform expressed is Nav1.4. In the animal model of CIM the Nav1.5 sodium channel isoform is upregulated, but the majority of sodium current is still carried by Nav1.4 sodium channels. Experiments using toxins to selectively bock the Nav1.4 isoform demonstrated that the cause of the hyperpolarized shift in sodium channel inactivation is a hyperpolarized shift in inactivation of the Nav1.4 isoform. These data suggest that CIM represents a new type of ion channel disease in which altered gating of sodium channels is due to improper regulation of the channels rather than mutation of channels or changes in isoform expression. The hypothesis that dysregulation of sodium channel gating underlies inexcitability of skeletal muscle in CIM raises the possibility that there maybe dysregulation of sodium channel gating in other tissues in critically ill patients. We propose that there is a syndrome of reduced electrical excitability in critically ill patients that affects skeletal muscle, peripheral nerve, the heart and central nervous system. This syndrome manifests as CIM, critical illness polyneuropathy, reduced cardiac contractility and septic encephalopathy.
Indexed as
Identifiers
16874452What OpenQuestion holds
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.