ArticleChannels (Austin, Tex.)2015
Cytosolic and nuclear calcium signaling in atrial myocytes: IP3-mediated calcium release and the role of mitochondria.
Article in Channels (Austin, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- From mitochondrial zonation to immune dysregulation: a mechanistic axis in diabetic cardiomyopathy.Frontiers in cardiovascular medicine · 2026Review
- Application of stereotactic radiotherapy in the treatment of cardiovascular diseases through sympathectomy.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- Role of Mitochondrial ROS for Calcium Alternans in Atrial Myocytes.Biomolecules · 2024Article
- Article
- Cardiac radiotherapy transiently alters left ventricular electrical properties and induces cardiomyocyte-specific ventricular substrate changes in heart failure.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 · 2023Article
- Nuclear Calcium in Cardiac (Patho)Physiology: Small Compartment, Big Impact.Biomedicines · 2023Review
- GBiomedicines · 2023Article
- The 'Reverse FDUF' Mechanism of Atrial Excitation-Contraction Coupling Sustains Calcium Alternans-A Hypothesis.Biomolecules · 2022Article
- Functional remodelling of perinuclear mitochondria alters nucleoplasmic CaPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Article
- Inositol 1,4,5-trisphosphate receptors in cardiomyocyte physiology and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Excitation-contraction coupling and calcium release in atrial muscle.Pflugers Archiv : European journal of physiology · 2021Review
- Dual SGLT-1 and SGLT-2 inhibition improves left atrial dysfunction in HFpEF.Cardiovascular diabetology · 2021Article
- CaMKIIδC Drives Early Adaptive CaCirculation research · 2020Article
- Mitochondrial calcium uniporter complex activation protects against calcium alternans in atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2020Article
- CaBiophysical journal · 2020Article
- Inositol 1,4,5-Trisphosphate Receptors in Human Disease: A Comprehensive Update.Journal of clinical medicine · 2020Review
- Calcium Signaling in Cardiomyocyte Function.Cold Spring Harbor perspectives in biology · 2020Review
- May the Force Not Be With You During Culture: Eliminating Mechano-Associated Feedback During Culture Preserves Cultured Atrial and Pacemaker Cell Functions.Frontiers in physiology · 2020Review
- Intrafibrillar and perinuclear mitochondrial heterogeneity in adult cardiac myocytes.Journal of molecular and cellular cardiology · 2019Article
- Crosstalk between FGF23- and angiotensin II-mediated CaCellular and molecular life sciences : CMLS · 2018Article
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Abstract
In rabbit atrial myocytes Ca signaling has unique features due to the lack of transverse (t) tubules, the spatial arrangement of mitochondria and the contribution of inositol-1,4,5-trisphosphate (IP3) receptor-induced Ca release (IICR). During excitation-contraction coupling action potential-induced elevation of cytosolic [Ca] originates in the cell periphery from Ca released from the junctional sarcoplasmic reticulum (j-SR) and then propagates by Ca-induced Ca release from non-junctional (nj-) SR toward the cell center. The subsarcolemmal region between j-SR and the first array of nj-SR Ca release sites is devoid of mitochondria which results in a rapid propagation of activation through this domain, whereas the subsequent propagation through the nj-SR network occurs at a velocity typical for a propagating Ca wave. Inhibition of mitochondrial Ca uptake with the Ca uniporter blocker Ru360 accelerates propagation and increases the amplitude of Ca transients (CaTs) originating from nj-SR. Elevation of cytosolic IP3 levels by rapid photolysis of caged IP3 has profound effects on the magnitude of subcellular CaTs with increased Ca release from nj-SR and enhanced CaTs in the nuclear compartment. IP3 uncaging restricted to the nucleus elicites 'mini'-Ca waves that remain confined to this compartment. Elementary IICR events (Ca puffs) preferentially originate in the nucleus in close physical association with membrane structures of the nuclear envelope and the nucleoplasmic reticulum. The data suggest that in atrial myocytes the nucleus is an autonomous Ca signaling domain where Ca dynamics are primarily governed by IICR.
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