ArticleJournal of molecular and cellular cardiology2012
Ankyrin-B reduction enhances Ca spark-mediated SR Ca release promoting cardiac myocyte arrhythmic activity.
Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- Reappraisal ofReviews in cardiovascular medicine · 2025Review
- Left Ventricular Non-Compaction, Atrial Fibrillation andJournal of clinical medicine research · 2025Article
- Dual ablation of the RyR2-Ser2808 and RyR2-Ser2814 sites increases propensity for pro-arrhythmic spontaneous CaThe Journal of physiology · 2024Article
- Loss of protein phosphatase 2A regulatory subunitFrontiers in cardiovascular medicine · 2024Article
- Alterations in Calcium Handling Are a Common Feature in an Arrhythmogenic Cardiomyopathy Cell Model Triggered by Desmosome Genes Loss.International journal of molecular sciences · 2023Article
- Role of CaArchives of toxicology · 2023Review
- Pleiotropic Ankyrins: Scaffolds for Ion Channels and Transporters.Channels (Austin, Tex.) · 2022Review
- Progressive Reduction in Right Ventricular Contractile Function Attributable to Altered Actin Expression in an Aging Mouse Model of Arrhythmogenic Cardiomyopathy.Circulation · 2022Article
- Mechanisms underlying the role of ankyrin-B in cardiac and neurological health and disease.Frontiers in cardiovascular medicine · 2022Review
- Regulation of Cardiac Contractility by the Alpha 2 Subunit of the NaFrontiers in physiology · 2022Review
- Regulation of Cardiac Conduction and Arrhythmias by Ankyrin/Spectrin-Based Macromolecular Complexes.Journal of cardiovascular development and disease · 2021Review
- Mechanisms and Alterations of Cardiac Ion Channels Leading to Disease: Role of Ankyrin-B in Cardiac Function.Biomolecules · 2020Review
- Calcium as a Key Player in Arrhythmogenic Cardiomyopathy: Adhesion Disorder or Intracellular Alteration?International journal of molecular sciences · 2019Review
- Protein Phosphatase 2A Regulates Cardiac NaCirculation research · 2019Article
- Downregulation of miR-146a Contributes to Cardiac Dysfunction Induced by the Tyrosine Kinase Inhibitor Sunitinib.Frontiers in pharmacology · 2019Article
- Ankyrin-B Q1283H Variant Linked to Arrhythmias Via Loss of Local Protein Phosphatase 2A Activity Causes Ryanodine Receptor Hyperphosphorylation.Circulation · 2018Article
- Spectrin-based pathways underlying electrical and mechanical dysfunction in cardiac disease.Expert review of cardiovascular therapy · 2018Article
- Hypokalemia-Induced Arrhythmias and Heart Failure: New Insights and Implications for Therapy.Frontiers in physiology · 2018Review
- The evolving role of ankyrin-B in cardiovascular disease.Heart rhythm · 2017Review
- Plakophilin-2 is required for transcription of genes that control calcium cycling and cardiac rhythm.Nature communications · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Ankyrin-B (AnkB) loss-of-function may cause ventricular arrhythmias and sudden cardiac death in humans. Cardiac myocytes from AnkB heterozygous mice (AnkB(+/-)) show reduced expression and altered localization of Na/Ca exchanger (NCX) and Na/K-ATPase (NKA), key players in regulating [Na](i) and [Ca](i). Here we investigate how AnkB reduction affects cardiac [Na](i), [Ca](i) and SR Ca release. We found reduced NCX and NKA transport function but unaltered [Na](i) and diastolic [Ca](i) in myocytes from AnkB(+/-) vs. wild-type (WT) mice. Ca transients, SR Ca content and fractional SR Ca release were larger in AnkB(+/-) myocytes. The frequency of spontaneous, diastolic Ca sparks (CaSpF) was significantly higher in intact myocytes from AnkB(+/-) vs. WT myocytes (with and without isoproterenol), even when normalized for SR Ca load. However, total ryanodine receptor (RyR)-mediated SR Ca leak (tetracaine-sensitive) was not different between groups. Thus, in AnkB(+/-) mice SR Ca leak is biased towards more Ca sparks (vs. smaller release events), suggesting more coordinated openings of RyRs in a cluster. This is due to local cytosolic RyR regulation, rather than intrinsic RyR differences, since CaSpF was similar in saponin-permeabilized myocytes from WT and AnkB(+/-) mice. The more coordinated RyRs openings resulted in an increased propensity of pro-arrhythmic Ca waves in AnkB(+/-) myocytes. In conclusion, AnkB reduction alters cardiac Na and Ca transport and enhances the coupled RyR openings, resulting in more frequent Ca sparks and waves although the total SR Ca leak is unaffected. This could enhance the propensity for triggered arrhythmias in AnkB(+/-) mice.
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Registered trials
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