ReviewFrontiers in physiology2015
Functional role of voltage gated Ca(2+) channels in heart automaticity.
Review in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.
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Who cites it
73 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- Circulating α-Klotho Levels in Relation to Cardiovascular Diseases: A Mendelian Randomization Study.Frontiers in endocrinology · 2022Pooled it
- Aging Disrupts L-type CaCirculation research · 2026Article
- Pacemaking in the heart: a redundant and robust system of mutually entrained oscillators driving cardiac automaticity.The Journal of physiology · 2026Review
- Upregulation of T-type voltage-dependent Ca²⁺ channels in activated hepatic stellate cells promotes liver fibrosis in metabolic dysfunction-associated steatohepatitis.Pflugers Archiv : European journal of physiology · 2026Article
- Autoimmune antibodies in arrhythmia: a narrative review of potential therapeutic targets to prevent overtreatment.Cardiovascular diagnosis and therapy · 2025Review
- Aging reduces the number and function of L-type calcium channels in the membrane of cardiac pacemaker cells.bioRxiv : the preprint server for biology · 2025Article
- Heart Rate Mystery Unveiled: Sex Differences in Human Sinoatrial Node Genes and Female Tachycardia.Circulation. Arrhythmia and electrophysiology · 2025Article
- The Neglected Internodal Tract-A Cardiac Conduction System Structure Homologous to the Development and Regulation of the Sinoatrial Node.Reviews in cardiovascular medicine · 2025Review
- Updates on Intrinsic Medicinal Chemistry of 1,4-dihydropyridines, Perspectives on Synthesis and Pharmacokinetics of Novel 1,4-dihydropyrimidines as Calcium Channel Blockers: Clinical Pharmacology.Current topics in medicinal chemistry · 2025Review
- Structure-Function Relationship of the Ryanodine Receptor Cluster Network in Sinoatrial Node Cells.Cells · 2024Article
- Selective blockade of CaNature communications · 2024Article
- Electrophysiological evaluation of the effect of peptide toxins on voltage-gated ion channels: a scoping review on theoretical and methodological aspects with focus on the Central and South American experience.The journal of venomous animals and toxins including tropical diseases · 2024Article
- Identifying sex similarities and differences in structure and function of the sinoatrial node in the mouse heart.Frontiers in medicine · 2024Article
- The Enigmas of Lymphatic Muscle Cells: Where Do They Come From, How Are They Maintained, and Can They Regenerate?Current rheumatology reviews · 2023Review
- Nr2f1a maintains atrialeLife · 2023Article
- Gene editing to prevent ventricular arrhythmias associated with cardiomyocyte cell therapy.Cell stem cell · 2023Article
- Pathophysiology of CaFrontiers in physiology · 2023Review
- Atrioventricular node dysfunction in pressure overload-induced heart failure-Involvement of the immune system and transcriptomic remodelling.Frontiers in pharmacology · 2023Article
- Heart rate reduction after genetic ablation of L-type CaFrontiers in cardiovascular medicine · 2023Article
- Disorder in Ca2+ release unit locations confers robustness but cuts flexibility of heart pacemaking.The Journal of general physiology · 2022Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pacemaker activity of automatic cardiac myocytes controls the heartbeat in everyday life. Cardiac automaticity is under the control of several neurotransmitters and hormones and is constantly regulated by the autonomic nervous system to match the physiological needs of the organism. Several classes of ion channels and proteins involved in intracellular Ca(2+) dynamics contribute to pacemaker activity. The functional role of voltage-gated calcium channels (VGCCs) in heart automaticity and impulse conduction has been matter of debate for 30 years. However, growing evidence shows that VGCCs are important regulators of the pacemaker mechanisms and play also a major role in atrio-ventricular impulse conduction. Incidentally, studies performed in genetically modified mice lacking L-type Cav1.3 (Cav1.3(-/-)) or T-type Cav3.1 (Cav3.1(-/-)) channels show that genetic inactivation of these channels strongly impacts pacemaking. In cardiac pacemaker cells, VGCCs activate at negative voltages at the beginning of the diastolic depolarization and importantly contribute to this phase by supplying inward current. Loss-of-function of these channels also impairs atrio-ventricular conduction. Furthermore, inactivation of Cav1.3 channels promotes also atrial fibrillation and flutter in knockout mice suggesting that these channels can play a role in stabilizing atrial rhythm. Genomic analysis demonstrated that Cav1.3 and Cav3.1 channels are widely expressed in pacemaker tissue of mice, rabbits and humans. Importantly, human diseases of pacemaker activity such as congenital bradycardia and heart block have been attributed to loss-of-function of Cav1.3 and Cav3.1 channels. In this article, we will review the current knowledge on the role of VGCCs in the generation and regulation of heart rate and rhythm. We will discuss also how loss of Ca(2+) entry through VGCCs could influence intracellular Ca(2+) handling and promote atrial arrhythmias.
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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.