scholarly journals Contributions of Ion Channels in Cardiac Arrhythmias

10.5772/31965 ◽  
2012 ◽  
Author(s):  
Jing Hongjuan ◽  
Zhang Lu
Keyword(s):  
Ion Channels ◽  
Cardiac Arrhythmias

scholarly journals A Thallium-Based Screening Procedure to Identify Molecules That Modulate the Activity of Ca2+-Activated Monovalent Cation-Selective Channels

2018 ◽  
Vol 23 (4) ◽  
pp. 341-352
Author(s):  
Koenraad Philippaert ◽  
Sara Kerselaers ◽  
Thomas Voets ◽  
Rudi Vennekens
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Cardiac Arrhythmias ◽  
Cell Types ◽  
Monovalent Cation ◽  
Screening Procedure ◽  
Channel Activity ◽  
Screening Assay

TRPM5 functions as a calcium-activated monovalent cation-selective ion channel and is expressed in a variety of cell types. Dysfunction of this type of channel has been recently implied in cardiac arrhythmias, diabetes, and other pathologies. Therefore, a growing interest has emerged to develop the pharmacology of these ion channels. We optimized a screening assay based on the thallium flux through the TRPM5 channel and a fluorescent thallium dye as a probe for channel activity. We show that this assay is capable of identifying molecules that inhibit or potentiate calcium-activated monovalent cation-selective ion channels.

Basic Cardiac Electrophysiology

2013 ◽  
pp. 171-190
Author(s):  
Hon-Chi Lee ◽  
Arshad Jahangir
Keyword(s):  
Ion Channels ◽  
Cardiac Arrhythmias ◽  
Action Potentials ◽  
Cardiac Electrophysiology ◽  
Structure And Function ◽  
Learning Objectives ◽  
Cardiac Ion Channels ◽  
Cardiac Action ◽  
And Function

The learning objectives of this chapter are to review some basic electrophysiologic concepts that are useful for the clinician. These include 1) the structure and function of cardiac ion channels; 2) the role of ion channels in the generation of cardiac action potentials; 3) the mechanisms of cardiac arrhythmias; and 4) inherited and acquired channelopathies.

New aspects in cardiac arrhythmias: the roll of ion channels and genetic aspects

2000 ◽  
Vol 89 (22) ◽  
pp. X2-X10 ◽  
Author(s):  
W. Haverkamp ◽  
L. Eckardt ◽  
P. Kirchhof ◽  
G. Mönnig ◽  
E. Schulze-Bahr ◽  
...  
Keyword(s):  
Ion Channels ◽  
Cardiac Arrhythmias

scholarly journals The anti-addictive drug ibogaine modulates voltage-gated ion channels and may trigger cardiac arrhythmias

2011 ◽  
Vol 11 (Suppl 2) ◽  
pp. A1 ◽  
Author(s):  
Michael Kovar ◽  
Xaver Koenig ◽  
Ágnes Mike ◽  
René Cervenka ◽  
Péter Lukács ◽  
...  
Keyword(s):  
Ion Channels ◽  
Cardiac Arrhythmias ◽  
Voltage Gated ◽  
Voltage Gated Ion Channels ◽  
Addictive Drug ◽  
Gated Ion Channels

Mechanistic and therapeutic perspectives for cardiac arrhythmias: beyond ion channels

2017 ◽  
Vol 60 (4) ◽  
pp. 348-355 ◽  
Author(s):  
Yufei Wu ◽  
Jun Li ◽  
Liang Xu ◽  
Li Lin ◽  
Yi-Han Chen
Keyword(s):  
Ion Channels ◽  
Cardiac Arrhythmias

Sudden infant death syndrome caused by cardiac arrhythmias: only a matter of genes encoding ion channels?

2016 ◽  
Vol 130 (2) ◽  
pp. 415-420 ◽  
Author(s):  
Georgia Sarquella-Brugada ◽  
Oscar Campuzano ◽  
Sergi Cesar ◽  
Anna Iglesias ◽  
Anna Fernandez ◽  
...  
Keyword(s):  
Ion Channels ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Cardiac Arrhythmias ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Genes Encoding

scholarly journals Caveolae, ion channels and cardiac arrhythmias

2008 ◽  
Vol 98 (2-3) ◽  
pp. 149-160 ◽  
Author(s):  
Ravi C. Balijepalli ◽  
Timothy J. Kamp
Keyword(s):  
Ion Channels ◽  
Cardiac Arrhythmias

Abstract 15963: Microrna Biophysically Modulates Cardiac Physiology via Directly Binding to Ion Channel

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Dandan Yang ◽  
Xiaoping Wan ◽  
Adrienne T Dennis ◽  
Emre Bektik ◽  
Zhihua Wang ◽  
...  
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Cardiac Arrhythmias ◽  
Cardiac Electrophysiology ◽  
Ex Vivo ◽  
Resting Membrane Potential ◽  
Seed Region ◽  
Cardiac Physiology ◽  
Long Term Effect ◽  
Evolutionarily Conserved

Background: Cardiac arrhythmias are a leading cause of morbidity and mortality. MicroRNAs (miRs) regulate the (electro) physiology of the heart and remodeling by canonical RNAi mechanism. Hypothesis: miRs maintain cardiac physiology also through noncanonical mechanisms. Methods: The physical binding between cardiac predominant miR--miR1 and ion channels was explored by EMSA, in situ PLA, RNA pull down and RIP assays. Electrophysiology of cardiomyocytes (CMs) and ex vivo miR1-deficient hearts were studied to reveal the functional outcome and the pathophysiological significance. Results: miR1 physically binds with an inward rectifier K + channel Kir2.1, which exists endogenously in CMs. This miR1-Kir2.1 binding is evolutionarily conserved. Functionally, miR1, at sub-pmol/L concentration, significantly suppresses IK1, depolarizes resting membrane potential, and prolongs final repolarization of action potentials in CMs. Mechanistically, miR1 binds to the pore-facing G-loop of Kir2.1 though the core sequence AAGAAG, which is outside the seed region. This biophysical modulation is involved in the dysregulation of a gain-of-function mutation Kir2.1-M301K in short-QT/AF patients. An AF-associated miR1-hSNP14A/G specifically disrupts the biophysical modulation while maintains miR1’s RNAi function. Significantly, miR1 but not hSNP14A/G eliminates the high inducibility of arrhythmia in miR1-deficient hearts. Conclusion: We reveal a novel function of miRs and develop a ground-breaking concept that endogenous miRs can physically bind with ion channels and rapidly modulate cardiac electrophysiology before its long-term effect of conventional RNAi mechanism. Our study provides more comprehensive understanding of ion-channel dysregulation associated with cardiac arrhythmias.

scholarly journals Defining new insight into atypical arrhythmia: a computational model of ankyrin-B syndrome

2010 ◽  
Vol 299 (5) ◽  
pp. H1505-H1514 ◽  
Author(s):  
Roseanne M. Wolf ◽  
Colleen C. Mitchell ◽  
Matthew D. Christensen ◽  
Peter J. Mohler ◽  
Thomas J. Hund
Keyword(s):  
Ion Channels ◽  
Sarcoplasmic Reticulum ◽  
Ion Channel ◽  
Cardiac Arrhythmia ◽  
Cardiac Arrhythmias ◽  
Molecular Mechanisms ◽  
Sinus Node ◽  
Cellular Level ◽  
Cytoskeletal Proteins ◽  
Ankyrin B

Normal cardiac excitability depends on the coordinated activity of specific ion channels and transporters within specialized domains at the plasma membrane and sarcoplasmic reticulum. Ion channel dysfunction due to congenital or acquired defects has been linked to human cardiac arrhythmia. More recently, defects in ion channel-associated proteins have been associated with arrhythmia. Ankyrin-B is a multifunctional adapter protein responsible for targeting select ion channels, transporters, cytoskeletal proteins, and signaling molecules in excitable cells, including neurons, pancreatic β-cells, and cardiomyocytes. Ankyrin-B dysfunction has been linked to cardiac arrhythmia in human patients and ankyrin-B heterozygous (ankyrin-B+/−) mice with a phenotype characterized by sinus node dysfunction, susceptibility to ventricular arrhythmias, and sudden death (“ankyrin-B syndrome”). At the cellular level, ankyrin-B+/− cells have defects in the expression and membrane localization of the Na+/Ca2+ exchanger and Na+-K+-ATPase, Ca2+ overload, and frequent afterdepolarizations, which likely serve as triggers for lethal cardiac arrhythmias. Despite knowledge gathered from mouse models and human patients, the molecular mechanism responsible for cardiac arrhythmias in the setting of ankyrin-B dysfunction remains unclear. Here, we use mathematical modeling to provide new insights into the cellular pathways responsible for Ca2+ overload and afterdepolarizations in ankyrin-B+/− cells. We show that the Na+/Ca2+ exchanger and Na+-K+-ATPase play related, yet distinct, roles in intracellular Ca2+ accumulation, sarcoplasmic reticulum Ca2+ overload, and afterdepolarization generation in ankyrin-B+/− cells. These findings provide important insights into the molecular mechanisms underlying a human disease and are relevant for acquired human arrhythmia, where ankyrin-B dysfunction has recently been identified.

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