ReviewJournal of muscle research and cell motility2002
Calcium regulation and muscle disease.
Review in Journal of muscle research and cell motility, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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
19 citing papers in PubMed, 60 citations in OpenAlex.
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- Nanodysferlins support membrane repair and binding to TRIM72/MG53 but do not localize to t-tubules or stabilize CaMolecular therapy. Methods & clinical development · 2024Article
- Skeletal muscle metabolic characteristics and fresh meat quality defects associated with wooden breast.Frontiers in physiology · 2024Review
- Bioengineered 3D Skeletal Muscle Model Reveals Complement 4b as a Cell-Autonomous Mechanism of Impaired Regeneration with Aging.Advanced materials (Deerfield Beach, Fla.) · 2023Article
- Using mass spectrometry imaging to visualize age-related subcellular disruption.Frontiers in molecular biosciences · 2023Review
- Efavirenz, atazanavir, and ritonavir disrupt sarcoplasmic reticulum CaAntiviral research · 2021Article
- CaOxidative medicine and cellular longevity · 2021Article
- The Role of Sarcolipin in Muscle Non-shivering Thermogenesis.Frontiers in physiology · 2018Article
- Endoplasmic reticulum calcium pumps and cancer cell differentiation.Biomolecules · 2012Article
- Successful use of albuterol in a patient with central core disease and mitochondrial dysfunction.Journal of inherited metabolic disease · 2010Article
- Loss of myotubularin function results in T-tubule disorganization in zebrafish and human myotubular myopathy.PLoS genetics · 2009Article
- Myopathy in Gaucher disease.Journal of inherited metabolic disease · 2008Article
- Stressed out: the skeletal muscle ryanodine receptor as a target of stress.The Journal of clinical investigation · 2008Review
- Article
- Inhibition of sarcoplasmic Ca2+-ATPase increases caffeine- and halothane-induced contractures in muscle bundles of malignant hyperthermia susceptible and healthy individuals.BMC anesthesiology · 2005Article
- Article
- Novel sarco(endo)plasmic reticulum proteins and calcium homeostasis in striated muscles.Journal of muscle research and cell motility · 2005Review
- Time-resolved charge translocation by sarcoplasmic reticulum Ca-ATPase measured on a solid supported membrane.Biophysical journal · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in intracellular Ca2+-concentration play an important role in the excitation-contraction-relaxation cycle of skeletal muscle. In this review we describe various inheritable muscle diseases to highlight the role of Ca2+-regulatory mechanisms. Upon excitation the ryanodine receptor releases Ca2+ in the cytosol. During and after contraction the sarcoplasmic reticulum (SR) Ca2+ATPase (SERCA) pumps Ca2+ back in the SR resulting in relaxation. An abnormal change in the intracellular Ca2+-concentration results in defective muscle contraction and/or relaxation, which is the cause of various muscle diseases. Malignant hyperthermia (MH) and central core disease (CCD) are both caused by mutations in the ryanodine receptor but show different clinical phenotypes. In MH an acute increase of Ca2+ results in excessive muscle contraction causing rigidity, while in CCD a chronic rise of cytosolic Ca2+ is seen, leading to mitochondrial damage, disorganization of myofibrils and muscle weakness. In Brody disease and also in mitochondrial myopathies, SERCA functions sub optimal causing a prolonged physiological Ca2+-elevation leading to slowing of relaxation. Defective actin-myosin interactions, as in nemaline myopathy and also in mitochondrial myopathies due to ATP-shortage, cause Ca2+-hyposensitivity and slowness of contraction. Information of Ca2+-kinetics in these inherited muscular diseases improves our understanding of the role of calcium in the physiology and pathophysiology of the skeletal muscle cell.
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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.