ReviewThe Journal of physiology2009
New roles of calsequestrin and triadin in cardiac muscle.
Review in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
59 citing papers in PubMed.
- Integrative Multi-Omics Analysis of Gill Responses to Long-Term Salinity Stress in Grass Carp (Antioxidants (Basel, Switzerland) · 2026Article
- Molecular genetics of skeletal muscle diseases associated with abnormal excitation-contraction coupling.Journal of human genetics · 2026Review
- The emerging role of calsequestrin 2: from calcium sensor and modulator to arrhythmia driver.Journal of physiology and biochemistry · 2026Review
- Congenital Long QT Syndrome: A Focus on Risk Stratification and Management.Reviews in cardiovascular medicine · 2025Review
- Induction of cardiac alternans in human iPS-derived cardiomyocytes through β-adrenergic receptor stimulation.Physiological reports · 2024Article
- The Structural-Functional Crosstalk of the Calsequestrin System: Insights and Pathological Implications.Biomolecules · 2023Review
- Cellular and electrophysiological characterization of triadin knockout syndrome using induced pluripotent stem cell-derived cardiomyocytes.Stem cell reports · 2023Article
- Multi-Omics Profiling of Hypertrophic Cardiomyopathy Reveals Altered Mechanisms in Mitochondrial Dynamics and Excitation-Contraction Coupling.International journal of molecular sciences · 2023Article
- Role of CaArchives of toxicology · 2023Review
- How does flecainide impact RyR2 channel function?The Journal of general physiology · 2022Article
- Transcriptional profiles of genes related to electrophysiological function in Scn5aPhysiological reports · 2021Article
- Excitation-contraction coupling and calcium release in atrial muscle.Pflugers Archiv : European journal of physiology · 2021Review
- Phylogenetic and biochemical analysis of calsequestrin structure and association of its variants with cardiac disorders.Scientific reports · 2020Article
- Interplay between Triadin and Calsequestrin in the Pathogenesis of CPVT in the Mouse.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Combinatorial Treatment of Human Cardiac Engineered Tissues With Biomimetic Cues Induces Functional Maturation as Revealed by Optical Mapping of Action Potentials and Calcium Transients.Frontiers in physiology · 2020Article
- Organellar Calcium Handling in the Cellular Reticular Network.Cold Spring Harbor perspectives in biology · 2019Review
- Two pools of IRE1α in cardiac and skeletal muscle cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Mechanistic insights from targeted molecular profiling of repolarization alternans in the intact human heart.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2019Article
- The intricacies of atrial calcium cycling during excitation-contraction coupling.The Journal of general physiology · 2017Review
- A novel mechanism of tandem activation of ryanodine receptors by cytosolic and SR luminal CaThe Journal of physiology · 2017Article
Corrections and comments
- Commented on by
- Commented on by
- Commented on by
Authors and funding
1 author.
Funding
Abstract
Cardiac calsequestrin (Casq2) and triadin are proteins located in specialized areas of the sarcoplasmic reticulum (SR) where the SR forms junctions with the sarcolemma (junctional SR). Casq2, triadin and junctin form a protein complex that is associated with cardiac ryanodine receptor 2 (RyR2) SR Ca(2+) release channels. This review highlights new insights of the roles of triadin and Casq2 derived from gene-targeted knock-out and knock-in mouse models that have recently become available. Characterization of the mouse models suggests that Casq2's contribution to SR Ca(2+) storage and release during excitation-contraction coupling is largely dispensable. Casq2's primary role appears to be in protecting the heart against premature Ca(2+) release and triggered arrhythmias. Furthermore, both cardiac Casq2 and triadin are important for the structural organization of the SR, which had previously not been recognized. In particular, ablation of triadin causes a 50% reduction in the extent of the junctional SR, which results in impaired excitation-contraction coupling at the level of the myocyte. While catecholamines could normalize contractile function by increasing I(Ca) and SR Ca(2+) content, it comes at the price of an increased risk for spontaneous Ca(2+) releases in triadin knock-out myocytes and catecholamine-induced ventricular arrhythmias in triadin knock-out mice.
Indexed as
Identifiers
What 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.