Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
New Insights into Cardiac Ion Channel Regulation 3.0
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

New Insights into Cardiac Ion Channel Regulation 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 November 2024) | Viewed by 7291

Special Issue Editors

Dr. Ademuyiwa S. Aromolaran

E-Mail Website
Guest Editor
Molecular Medicine Program, Department of Surgery, Division of Cardiothoracic Surgery, Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT 84112, USA
Interests: cardiac electrophysiology; ion channel biophysics; arrhythmias; inflammation and metabolic disorders
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Brian P. Delisle

E-Mail Website
Co-Guest Editor
Department of Physiology, University of Kentucky, Lexington, KY 40536, USA
Interests: genetics; ion channel; protein trafficking; cardiac arrhythmia; chronobiology; protein structure and function
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The ordered electrical excitation of the heart coordinates the efficient pumping of blood throughout the body. Cardiac arrhythmias are electrical disturbances that are often the manifestation of drug toxicity or acquired or genetic diseases. Clinicians and scientists collectively work to identify the basis and prevention of different arrhythmogenic mechanisms. Molecular, cellular, animal, and clinical studies have identified several major families of clinically important cardiac ionic currents and their associated genes and proteins. These studies have led to new discoveries in ion channel regulation at the level of gene transcription, mRNA splicing and stability, translation, protein assembly, intracellular transport (trafficking), second messenger modification, and biophysical function. In this Special Issue, we focus on foundational and emerging concepts in cardiac ion channel regulation, with an emphasis on how this information contributes to a better understanding of normal cardiac excitation and arrhythmogenicity.

Dr. Ademuyiwa S. Aromolaran
Prof. Dr. Brian P. Delisle
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Related Special Issues

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

14 pages, 2475 KiB  
Article
Beta-Adrenergic Activation of the Inward Rectifier K+ Current Is Mediated by the CaMKII Pathway in Canine Ventricular Cardiomyocytes
by Zsigmond Máté Kovács, Balázs Horváth, Csaba Dienes, József Óvári, Dénes Kiss, Tamás Hézső, Norbert Szentandrássy, János Magyar, Tamás Bányász and Péter Pál Nánási
Int. J. Mol. Sci. 2024, 25(21), 11609; https://doi.org/10.3390/ijms252111609 - 29 Oct 2024
Viewed by 464
Abstract
Several ion currents in the mammalian ventricular myocardium are substantially regulated by the sympathetic nervous system via β-adrenergic receptor activation, including the slow delayed rectifier K+ current and the L-type calcium current. This study investigated the downstream mechanisms of β-adrenergic receptor stimulation [...] Read more.
Several ion currents in the mammalian ventricular myocardium are substantially regulated by the sympathetic nervous system via β-adrenergic receptor activation, including the slow delayed rectifier K+ current and the L-type calcium current. This study investigated the downstream mechanisms of β-adrenergic receptor stimulation by isoproterenol (ISO) on the inward rectifier (IK1) and the rapid delayed rectifier (IKr) K+ currents using action potential voltage clamp (APVC) and conventional voltage clamp techniques in isolated canine left ventricular cardiomyocytes. IK1 and IKr were dissected by 50 µM BaCl2 and 1 µM E-4031, respectively. Acute application of 10 nM ISO significantly increased IK1 under the plateau phase of the action potential (0–+20 mV) using APVC, and similar results were obtained with conventional voltage clamp. However, β-adrenergic receptor stimulation did not affect the peak current density flowing during terminal repolarization or the overall IK1 integral. The ISO-induced enhancement of IK1 was blocked by the calcium/calmodulin kinase II (CaMKII) inhibitor KN-93 (1 µM) but not by the protein kinase A inhibitor H-89 (3 µM). Neither KN-93 nor H-89 affected the IK1 density under baseline conditions (in the absence of ISO). In contrast, parameters of the IKr current were not affected by β-adrenergic receptor stimulation with ISO. These findings suggest that sympathetic activation enhances IK1 in canine left ventricular cells through the CaMKII pathway, while IKr remains unaffected under the experimental conditions used. Full article
(This article belongs to the Special Issue New Insights into Cardiac Ion Channel Regulation 3.0)
►▼ Show Figures

Figure 1

22 pages, 5578 KiB  
Article
Human Sinoatrial Node Pacemaker Activity: Role of the Slow Component of the Delayed Rectifier K+ Current, IKs
by Arie O. Verkerk and Ronald Wilders
Int. J. Mol. Sci. 2023, 24(8), 7264; https://doi.org/10.3390/ijms24087264 - 14 Apr 2023
Cited by 3 | Viewed by 2092
Abstract
The pacemaker activity of the sinoatrial node (SAN) has been studied extensively in animal species but is virtually unexplored in humans. Here we assess the role of the slowly activating component of the delayed rectifier K+ current (IKs) in human [...] Read more.
The pacemaker activity of the sinoatrial node (SAN) has been studied extensively in animal species but is virtually unexplored in humans. Here we assess the role of the slowly activating component of the delayed rectifier K+ current (IKs) in human SAN pacemaker activity and its dependence on heart rate and β-adrenergic stimulation. HEK-293 cells were transiently transfected with wild-type KCNQ1 and KCNE1 cDNA, encoding the α- and β-subunits of the IKs channel, respectively. KCNQ1/KCNE1 currents were recorded both during a traditional voltage clamp and during an action potential (AP) clamp with human SAN-like APs. Forskolin (10 µmol/L) was used to increase the intracellular cAMP level, thus mimicking β-adrenergic stimulation. The experimentally observed effects were evaluated in the Fabbri–Severi computer model of an isolated human SAN cell. Transfected HEK-293 cells displayed large IKs-like outward currents in response to depolarizing voltage clamp steps. Forskolin significantly increased the current density and significantly shifted the half-maximal activation voltage towards more negative potentials. Furthermore, forskolin significantly accelerated activation without affecting the rate of deactivation. During an AP clamp, the KCNQ1/KCNE1 current was substantial during the AP phase, but relatively small during diastolic depolarization. In the presence of forskolin, the KCNQ1/KCNE1 current during both the AP phase and diastolic depolarization increased, resulting in a clearly active KCNQ1/KCNE1 current during diastolic depolarization, particularly at shorter cycle lengths. Computer simulations demonstrated that IKs reduces the intrinsic beating rate through its slowing effect on diastolic depolarization at all levels of autonomic tone and that gain-of-function mutations in KCNQ1 may exert a marked bradycardic effect during vagal tone. In conclusion, IKs is active during human SAN pacemaker activity and has a strong dependence on heart rate and cAMP level, with a prominent role at all levels of autonomic tone. Full article
(This article belongs to the Special Issue New Insights into Cardiac Ion Channel Regulation 3.0)
►▼ Show Figures

Figure 1

Review

Jump to: Research

14 pages, 1863 KiB  
Review
Impact of Impaired Kidney Function on Arrhythmia-Promoting Cardiac Ion Channel Regulation
by Frederick Sinha, Frank Schweda, Lars S. Maier and Stefan Wagner
Int. J. Mol. Sci. 2023, 24(18), 14198; https://doi.org/10.3390/ijms241814198 - 17 Sep 2023
Viewed by 2131
Abstract
Chronic kidney disease (CKD) is associated with a significantly increased risk of cardiovascular events and sudden cardiac death. Although arrhythmias are one of the most common causes of sudden cardiac death in CKD patients, the molecular mechanisms involved in the development of arrhythmias [...] Read more.
Chronic kidney disease (CKD) is associated with a significantly increased risk of cardiovascular events and sudden cardiac death. Although arrhythmias are one of the most common causes of sudden cardiac death in CKD patients, the molecular mechanisms involved in the development of arrhythmias are still poorly understood. In this narrative review, therefore, we summarize the current knowledge on the regulation of cardiac ion channels that contribute to arrhythmia in CKD. We do this by first explaining the excitation–contraction coupling, outlining current translational research approaches, then explaining the main characteristics in CKD patients, such as abnormalities in electrolytes and pH, activation of the autonomic nervous system, and the renin–angiotensin–aldosterone system, as well as current evidence for proarrhythmic properties of uremic toxins. Finally, we discuss the substance class of sodium–glucose co-transporter 2 inhibitors (SGLT2i) on their potential to modify cardiac channel regulation in CKD and, therefore, as a treatment option for arrhythmias. Full article
(This article belongs to the Special Issue New Insights into Cardiac Ion Channel Regulation 3.0)
►▼ Show Figures

Figure 1

14 pages, 1557 KiB  
Review
Relevance of KCNJ5 in Pathologies of Heart Disease
by Karisa M. Meyer, Nipun Malhotra, Jung seo Kwak and Mona El Refaey
Int. J. Mol. Sci. 2023, 24(13), 10849; https://doi.org/10.3390/ijms241310849 - 29 Jun 2023
Cited by 3 | Viewed by 1809
Abstract
Abnormalities in G-protein-gated inwardly rectifying potassium (GIRK) channels have been implicated in diseased states of the cardiovascular system; however, the role of GIRK4 (Kir3.4) in cardiac physiology and pathophysiology has yet to be completely understood. Within the heart, the KACh channel, consisting [...] Read more.
Abnormalities in G-protein-gated inwardly rectifying potassium (GIRK) channels have been implicated in diseased states of the cardiovascular system; however, the role of GIRK4 (Kir3.4) in cardiac physiology and pathophysiology has yet to be completely understood. Within the heart, the KACh channel, consisting of two GIRK1 and two GIRK4 subunits, plays a major role in modulating the parasympathetic nervous system’s influence on cardiac physiology. Being that GIRK4 is necessary for the functional KACh channel, KCNJ5, which encodes GIRK4, it presents as a therapeutic target for cardiovascular pathology. Human variants in KCNJ5 have been identified in familial hyperaldosteronism type III, long QT syndrome, atrial fibrillation, and sinus node dysfunction. Here, we explore the relevance of KCNJ5 in each of these diseases. Further, we address the limitations and complexities of discerning the role of KCNJ5 in cardiovascular pathophysiology, as identical human variants of KCNJ5 have been identified in several diseases with overlapping pathophysiology. Full article
(This article belongs to the Special Issue New Insights into Cardiac Ion Channel Regulation 3.0)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop