ArticleJournal of the American Heart Association2017
Redox and Activation of Protein Kinase A Dysregulates Calcium Homeostasis in Pulmonary Vein Cardiomyocytes of Chronic Kidney Disease.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Modulated Calcium Homeostasis and Release Events Under Atrial Fibrillation and Its Risk Factors: A Meta-Analysis.Frontiers in cardiovascular medicine · 2021Pooled it
- Phosphodiesterase 10A Inhibitor Modulates Right Ventricular Outflow Tract Electrophysiological Activities and Calcium Homeostasis via the cGMP/PKG Pathway.Journal of cellular and molecular medicine · 2025Article
- Targeting NLRP3 signaling reduces myocarditis-induced arrhythmogenesis and cardiac remodeling.Journal of biomedical science · 2024Article
- Pro-Arrhythmic Potential of Accumulated Uremic Toxins Is Mediated via Vulnerability of Action Potential Repolarization.International journal of molecular sciences · 2023Article
- Review
- Ziprasidone Induces Rabbit Atrium Arrhythmogenesis via Modification of Oxidative Stress and Sodium/Calcium Homeostasis.Biomedicines · 2022Article
- Calcium dysregulation increases right ventricular outflow tract arrhythmogenesis in rabbit model of chronic kidney disease.Journal of cellular and molecular medicine · 2021Article
- ROS‑associated mechanism of different concentrations of pinacidil postconditioning in the rat cardiac Nrf2‑ARE signaling pathway.Molecular medicine reports · 2021Article
- Fibroblast Growth Factor 1 Reduces Pulmonary Vein and Atrium ArrhythmogenesisFrontiers in cardiovascular medicine · 2021Article
- The effect of Sirt1 deficiency on CaJournal of cellular and molecular medicine · 2020Article
- Cardiac calcium dysregulation in mice with chronic kidney disease.Journal of cellular and molecular medicine · 2020Article
- Examining Cardiomyocyte Dysfunction Using Acute Chemical Induction of an Ageing Phenotype.International journal of molecular sciences · 2019Article
- Chronic kidney disease-induced atrial structural remodeling and atrial fibrillation: more studies on the pathological mechanism are encouraged.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic kidney disease (CKD) increases the occurrence of atrial fibrillation and pulmonary vein (PV) arrhythmogenesis. Calcium dysregulation and reactive oxygen species (ROS) enhance PV arrhythmogenic activity. The purposes of this study were to investigate whether CKD modulates PV electrical activity through dysregulation of calcium homeostasis and ROS. METHODS AND
resultsBiochemical and electrocardiographic studies were conducted in rabbits with and without CKD (induced by 150 mg/kg per day neomycin sulfate and 500 mg/kg per day cefazolin). Confocal microscopy with fluorescence and a whole-cell patch clamp were applied to study calcium homeostasis and electrical activities in control and CKD isolated single PV cardiomyocytes with or without treatment with H89 (1 μmol/L, a protein kinase A inhibitor) and MPG (N-[2-mercaptopropionyl]glycine; 100 μmol/L, a ROS scavenger). The ROS in mitochondria and cytosol were evaluated via intracellular dye fluorescence and lipid peroxidation. CKD rabbits had excessive atrial premature captures over those of control rabbits. Compared with the control, CKD PV cardiomyocytes had a faster beating rate and larger calcium transient amplitudes, sarcoplasmic reticulum calcium contents, sodium/calcium exchanger currents, and late sodium currents but smaller L-type calcium current densities. CKD PV cardiomyocytes had a higher frequency and longer duration of calcium sparks and more ROS in the mitochondria and cytosol than did controls. Moreover, H89 suppressed all calcium sparks in CKD PV cardiomyocytes, and H89- and MPG-treated CKD PV cardiomyocytes had similar calcium transients compared with control PV cardiomyocytes.
conclusionsCKD increases PV arrhythmogenesis with enhanced calcium-handling abnormalities through activation of protein kinase A and ROS.
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