ReviewBioscience reports2022
Skeletal and cardiac muscle calcium transport regulation in health and disease.
Review in Bioscience reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 42 citations in OpenAlex.
- Differentiated skeletal myotubes coupled with bimodal biosensing for dynamic functional evaluation of inflammatory myotube dysfunction.Microsystems & nanoengineering · 2026Article
- Inactivation of SERCA2 at Cys674 induces skeletal muscle atrophy by activating the TGFβ/Smad-S100a4 axis to promote inflammation.Redox biology · 2026Article
- Ryanodine Receptor CaActa physiologica (Oxford, England) · 2026Article
- Sarcolipin but not phospholamban responds toFrontiers in physiology · 2026Article
- From calcium pump to metabolic hub: emerging genetic phenotypes and metabolic networks of SERCA2 in skeletal muscle.Frontiers in physiology · 2026Review
- Associations of high protein supplements with gut microbiota and skeletal muscle mass in hospitalized older people.BMC geriatrics · 2025Article
- Transcription factor MITF regulates masseter muscle growth and development.Physiological reports · 2025Article
- Neuroprotection in neonatal Hypoxia-ischaemia: melatonin targets NCX1 to inhibit mitochondrial autophagy via the PINK1-Parkin pathway.Journal of molecular histology · 2025Article
- Wnt/β-catenin pathway induces cardiac dysfunction via AKAP6-mediated RyR2 phosphorylation and sarcoplasmic reticulum calcium leakage.Journal of molecular cell biology · 2025Article
- Allicin ameliorates acute myocardial infarction in rats by modulating calcium homeostasis in cardiomyocytes through the induction of hydrogen sulfide production.Frontiers in pharmacology · 2025Article
- Current state of heart failure treatment: are mesenchymal stem cells and their exosomes a future therapy?Frontiers in cardiovascular medicine · 2025Review
- Mechanistic Relevance of Ventricular Arrhythmias in Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
- TheMetabolites · 2024Article
- The Cardiomyocyte in Cirrhosis: Pathogenic Mechanisms Underlying Cirrhotic Cardiomyopathy.Reviews in cardiovascular medicine · 2024Review
- Whole-genome SNP allele frequency differences between Tibetan and Large white pigs reveal genes associated with skeletal muscle growth.BMC genomics · 2024Article
- Low Muscle Mass Is Associated with Poorer Glycemic Control and Higher Oxidative Stress in Older Patients with Type 2 Diabetes.Nutrients · 2023Article
- Dysregulated Calcium Handling in Cirrhotic Cardiomyopathy.Biomedicines · 2023Review
- Calcium Homeostasis, Transporters, and Blockers in Health and Diseases of the Cardiovascular System.International journal of molecular sciences · 2023Review
- Whole Transcriptome Analysis of Differentially Expressed Genes in Cultured Nile Tilapia (Genes · 2023Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In healthy muscle, the rapid release of calcium ions (Ca2+) with excitation-contraction (E-C) coupling, results in elevations in Ca2+ concentrations which can exceed 10-fold that of resting values. The sizable transient changes in Ca2+ concentrations are necessary for the activation of signaling pathways, which rely on Ca2+ as a second messenger, including those involved with force generation, fiber type distribution and hypertrophy. However, prolonged elevations in intracellular Ca2+ can result in the unwanted activation of Ca2+ signaling pathways that cause muscle damage, dysfunction, and disease. Muscle employs several calcium handling and calcium transport proteins that function to rapidly return Ca2+ concentrations back to resting levels following contraction. This review will detail our current understanding of calcium handling during the decay phase of intracellular calcium transients in healthy skeletal and cardiac muscle. We will also discuss how impairments in Ca2+ transport can occur and how mishandling of Ca2+ can lead to the pathogenesis and/or progression of skeletal muscle myopathies and cardiomyopathies.
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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.