ArticleCardiovascular research2012
Ultrastructural remodelling of Ca(2+) signalling apparatus in failing heart cells.
Article in Cardiovascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- Early Stage Morphogenesis of Transverse Tubules in Rat Cardiomyocytes: The Role of pBIN1.Circulation research · 2025Article
- Structure, Function, and Regulation of the Junctophilin Family.Annual review of physiology · 2024Review
- Article
- DNA Methylation Analysis Identifies Novel Epigenetic Loci in Dilated Murine Heart upon Exposure to Volume Overload.International journal of molecular sciences · 2023Article
- Electron microscopy of cardiac 3D nanodynamics: form, function, future.Nature reviews. Cardiology · 2022Review
- The role of junctophilin proteins in cellular function.Physiological reviews · 2022Review
- CMYA5 establishes cardiac dyad architecture and positioning.Nature communications · 2022Article
- Towards precision medicine in heart failure.Nature reviews. Cardiology · 2021Review
- Titin M-line insertion sequence 7 is required for proper cardiac function in mice.Journal of cell science · 2021Article
- Transcriptional regulation of intermolecular CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- In silico simulations reveal that RYR distribution affects the dynamics of calcium release in cardiac myocytes.The Journal of general physiology · 2021Article
- Junctophilin-2 tethers T-tubules and recruits functional L-type calcium channels to lipid rafts in adult cardiomyocytes.Cardiovascular research · 2021Article
- Nanoscale Organization, Regulation, and Dynamic Reorganization of Cardiac Calcium Channels.Frontiers in physiology · 2021Review
- The Physiology and Pathophysiology of T-Tubules in the Heart.Frontiers in physiology · 2021Review
- Structural variability of dyads relates to calcium release in rat ventricular myocytes.Scientific reports · 2020Article
- Calcium Signaling in Cardiomyocyte Function.Cold Spring Harbor perspectives in biology · 2020Review
- Lingguizhugan decoction attenuates doxorubicin-induced heart failure in rats by improving TT-SR microstructural remodeling.BMC complementary and alternative medicine · 2019Article
- Junctophilin-2 expression rescues atrial dysfunction through polyadic junctional membrane complex biogenesis.JCI insight · 2019Article
- E-C coupling structural protein junctophilin-2 encodes a stress-adaptive transcription regulator.Science (New York, N.Y.) · 2018Article
- Size Matters: Ryanodine Receptor Cluster Size Affects Arrhythmogenic Sarcoplasmic Reticulum Calcium Release.Journal of the American Heart Association · 2018Article
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13 authors.
Funding
Abstract
aimsThe contraction of a heart cell is controlled by Ca(2+)-induced Ca(2+) release between L-type Ca(2+) channels (LCCs) in the cell membrane/T-tubules (TTs) and ryanodine receptors (RyRs) in the junctional sarcoplasmic reticulum (SR). During heart failure, LCC-RyR signalling becomes defective. The purpose of the present study was to reveal the ultrastructural mechanism underlying the defective LCC-RyR signalling and contractility. METHODS AND
resultsIn rat models of heart failure produced by transverse aortic constriction surgery, stereological analysis of transmission electron microscopic images showed that the volume density and the surface area of junctional SRs and those of SR-coupled TTs were both decreased in failing heart cells. The TT-SR junctions were displaced or missing from the Z-line areas. Moreover, the spatial span of individual TT-SR junctions was markedly reduced in failing heart cells. Numerical simulation and junctophilin-2 knockdown experiments demonstrated that the decrease in junction size (and thereby the constitutive LCC and RyR numbers) led to a scattered delay of Ca(2+) release activation.
conclusionsThe shrinking and eventual absence of TT-SR junctions are important mechanisms underlying the desynchronized and inhomogeneous Ca(2+) release and the decreased contractile strength in heart failure. Maintaining the nanoscopic integrity of TT-SR junctions thus represents a therapeutic strategy against heart failure and related cardiomyopathies.
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