ReviewJournal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing2015
The genetic basis for inherited forms of sinoatrial dysfunction and atrioventricular node dysfunction.
Review in Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Aging Disrupts L-type CaCirculation research · 2026Article
- Hypokalaemia and bradycardia unmask the loss-of-function phenotype of a Brugada Syndrome SCN5A mutation.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 · 2026Article
- A rare HCN4 variant combined with sick sinus syndrome, left ventricular noncompaction, and complex congenital heart disease.Channels (Austin, Tex.) · 2025Article
- 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
- Modeling the atrioventricular conduction axis using human pluripotent stem cell-derived cardiac assembloids.Cell stem cell · 2024Article
- Pacemaker Channels and the Chronotropic Response in Health and Disease.Circulation research · 2024Review
- Fuel source shift or cost reduction: Context-dependent adaptation strategies in closely relatedZoological research · 2022Article
- Diagnostic Yield of Genetic Testing in Young Patients With Atrioventricular Block of Unknown Cause.Journal of the American Heart Association · 2022Article
- The Bradycardic Agent Ivabradine Acts as an Atypical Inhibitor of Voltage-Gated Sodium Channels.Frontiers in pharmacology · 2022Article
- Aging Alters the Formation and Functionality of Signaling Microdomains Between L-type Calcium Channels and β2-Adrenergic Receptors in Cardiac Pacemaker Cells.Frontiers in physiology · 2022Article
- Altered microRNA and mRNA profiles during heart failure in the human sinoatrial node.Scientific reports · 2021Article
- Intracellular NaInternational journal of molecular sciences · 2021Article
- Impaired neuronal sodium channels cause intranodal conduction failure and reentrant arrhythmias in human sinoatrial node.Nature communications · 2020Article
- Mutations in NaFrontiers in physiology · 2019Article
- NovelFrontiers in genetics · 2019Article
- Current understanding of the pathophysiological mechanisms responsible for inappropriate sinus tachycardia: role of the If "funny" current.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2016Review
- Therapeutic Approaches to Genetic Ion Channelopathies and Perspectives in Drug Discovery.Frontiers in pharmacology · 2016Review
- Protective effects of kaempferol against cardiac sinus node dysfunction via CaMKII deoxidization.Anatomy & cell biology · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sinoatrial node (SAN) and the atrioventricular node (AVN) are the anatomical and functional regions of the heart which play critical roles in the generation and conduction of the electrical impulse. Their functions are ensured by peculiar structural cytological properties and specific collections of ion channels. Impairment of SAN and AVN activity is generally acquired,but in some cases familial inheritance has been established and therefore a genetic cause is involved. In recent years, combined efforts of clinical practice and experimental basic science studies have identified and characterized several causative gene mutations associated with the nodal syndromes. Channelopathies, i.e., diseases associated with defective ion channels, remain the major cause of genetically determined nodal arrhythmias; however, it is becoming increasingly evident that mutations in other classes of regulatory and structural proteins also have profound pathophysiological roles. In this review, we will present some aspects of the genetic identification of the molecular mechanism underlying both SAN and AVN dysfunctions with a particular focus on mutations of the Na, pacemaker (HCN), and Ca channels. Genetic defects in regulatory proteins and calcium-handling proteins will be also considered. In conclusion, the identification of the genetic defects associated with familial nodal dysfunction is an essential step for implementing an appropriate therapeutic treatment.
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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.