ReviewCardiovascular research2013
Triadin regulates cardiac muscle couplon structure and microdomain Ca(2+) signalling: a path towards ventricular arrhythmias.
Review in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 54 citations in OpenAlex.
- Structural and Functional Regulation of RyR2 in Cardiac Calcium Handling and Arrhythmogenesis.Biomedicines · 2026Review
- Mechanistic Insights into Glucocorticoid-Induced Ocular Hypertension Using Differences in Mouse Strain Responsiveness.The American journal of pathology · 2026Article
- Alternative splicing dynamics during human cardiac development in vivo and in vitro.Stem cell reports · 2026Article
- Article
- Catecholaminergic polymorphic ventricular tachycardia and early-onset atrial fibrillation in a tactical athlete with a heterozygous truncating variant inHeartRhythm case reports · 2025Article
- Application of integrated omics in aseptic loosening of prostheses after hip replacement.Molecular medicine reports · 2025Article
- A Single-Cell Atlas of Porcine Skeletal Muscle Reveals Mechanisms That Regulate Intramuscular Adipogenesis.International journal of molecular sciences · 2024Article
- A Catalogue of Structural Variation across Ancestrally Diverse Asian Genomes.Nature communications · 2024Article
- The Dysfunction of CaInternational journal of molecular sciences · 2023Review
- Genome-Wide Assessment of Runs of Homozygosity by Whole-Genome Sequencing in Diverse Horse Breeds Worldwide.Genes · 2023Article
- Cellular and electrophysiological characterization of triadin knockout syndrome using induced pluripotent stem cell-derived cardiomyocytes.Stem cell reports · 2023Article
- Calcium Handling in Inherited Cardiac Diseases: A Focus on Catecholaminergic Polymorphic Ventricular Tachycardia and Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2023Review
- Defect in cytosolic Neu2 sialidase abrogates lipid metabolism and impairs muscle function in vivo.Scientific reports · 2022Article
- Impaired Binding to Junctophilin-2 and Nanostructural Alteration in CPVT Mutation.Circulation research · 2021Article
- T-tubule remodeling in human hypertrophic cardiomyopathy.Journal of muscle research and cell motility · 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
- Calcium as a Key Player in Arrhythmogenic Cardiomyopathy: Adhesion Disorder or Intracellular Alteration?International journal of molecular sciences · 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
- Caveolae-Specific CaMKII Signaling in the Regulation of Voltage-Dependent Calcium Channel and Cardiac Hypertrophy.Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Since the discovery of triadin >20 years ago as one of the major proteins located in the junctional sarcoplasmic reticulum, the field has come a long way in understanding the pivotal role of triadin in orchestrating sarcoplasmic reticulum Ca(2+)-release and hence excitation-contraction (EC) coupling. Building on the information gathered from earlier lipid bilayer and myocyte overexpression studies, the gene-targeted ablation of Trdn demonstrated triadin's indispensable role for maintaining the structural integrity of the couplon. More recently, the discovery of inherited and acquired diseases displaying altered expression and function of triadin has further emphasized the role of triadin in health and disease. Novel therapeutic approaches could be aimed at correcting the loss of triadin in diseased hearts, and thereby correcting the sub-cellular EC coupling defect. This review summarizes current concepts of the impact of triadin on cardiac EC coupling with a focus towards triadin's role for ventricular arrhythmia.
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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.