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Cells
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Advances in Ion Channel Biology: From Molecular Mechanisms to Therapeutic...
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Advances in Ion Channel Biology: From Molecular Mechanisms to Therapeutic Targets

A Special Issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 November 2026 | Viewed by 1028

Editors

Dr. Shridhar Sanghvi

E-Mail Website
Guest Editor
Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH, USA
Interests: cardiac physiology; calcium signaling; excitation–contraction coupling; intracellular ion channels; electrophysiology; channelopathies; bioenergetics; stem cells
Dr. Yang Zheng

E-Mail Website
Guest Editor
Department of Basic Medical Sciences, University of Arizona College of Medicine, Phoenix, CA, USA
Interests: cardiac electrophysiology; arrhythmias; heart failure; cardiac ion channels; channelopathies
Dr. Md Shahidul Islam

E-Mail Website
Guest Editor
1. Karolinska Institutet, Department of Clinical Sciences and Education, Södersjukhuset, Research Center, 5th Floor, SE-118 83 Stockholm, Sweden
2. Department of Internal Medicine, Uppsala University Hospital, SE-751 85 Uppsala, Sweden
Interests: islet biology; pancreatic beta cells; insulin secretion; glucagon-like peptide 1; calcium signaling; TRP channels; diabetes; signal transduction in beta-cells; stimulus–secretion coupling; calcium signaling in the beta cells; ryanodine receptors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ion channels are fundamental in cellular physiology, governing processes from neuronal signaling and muscle contraction to hormone secretion and immune responses. Over the last decade, advances in structural biology, electrophysiology, and computational modeling have dramatically expanded our understanding of ion channel function, regulation, and pharmacology. This Special Issue will bring together cutting-edge studies that highlight the dynamic and multifaceted nature of ion channels in health and disease.

Recent breakthroughs in cryo-electron microscopy have unveiled the high-resolution structures of previously elusive channel complexes, offering unprecedented insights into gating mechanisms and drug-binding sites. Concurrently, novel genetic and optogenetic tools have enabled the precise manipulation of channel activity in vivo, strengthening our grasp of their physiological roles. Moreover, the discovery of new channelopathies has underscored the clinical relevance of ion channels, spurring efforts to develop targeted therapies.

For this Special Issue, we welcome submissions in the form of original research articles and reviews providing insights into spanning molecular mechanisms, biophysical innovations, and translational applications in ion channel research. By integrating diverse perspectives, we aim to inspire a deeper appreciation of ion channels as both intricate molecular machines and promising therapeutic targets.

Dr. Shridhar Sanghvi
Dr. Yang Zheng
Dr. Md Shahidul Islam
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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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.

Keywords

  • ion channels
  • electrophysiology
  • cryo-electron microscopy
  • channelopathy
  • membrane protein
  • gating mechanism
  • structural biology

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Published Papers (1 paper)

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Research

11 pages, 2650 KB  
Article
Expression Defects of SCN5A Common Polymorphisms S524Y and H558R in the Q1077 Splice Variant Can Be Rescued by Mexiletine
by Rou-Mu Hu, Evelyn J. Song, Carmen R. Valdivia, Isabelle Deschenes, Jonathan C. Makielski and Bi-Hua Tan
Cells 2026, 15(15), 1418; https://doi.org/10.3390/cells15151418 - 5 Aug 2026
Viewed by 439
Abstract
The cardiac sodium channel NaV1.5, encoded by SCN5A, generates the inward sodium current required for myocardial excitability and impulse conduction. Loss-of-function mutations of NaV1.5 have been implicated in inherited arrhythmia syndromes, including Brugada syndrome, progressive cardiac conduction disease, and [...] Read more.
The cardiac sodium channel NaV1.5, encoded by SCN5A, generates the inward sodium current required for myocardial excitability and impulse conduction. Loss-of-function mutations of NaV1.5 have been implicated in inherited arrhythmia syndromes, including Brugada syndrome, progressive cardiac conduction disease, and congenital sick sinus syndrome. The common SCN5A polymorphism H558R has reported minor allele frequencies ranging from 9.2% to 29% across ethnic groups, whereas S524Y has been described in individuals of African ancestry with a minor allele frequency of approximately 3.3%. Two splice variants of human SCN5A, one lacking a glutamine at position 1077 (Q1077del) and one containing Q1077, exist in every human in a 2:1 mRNA transcript ratio. We engineered these two polymorphisms in both backgrounds and reported that when S524Y and H558R were expressed in the Q1077del variant, current densities were normal. In the Q1077 variant, however, the current densities showed a dramatic reduction compared to those in the Q1077del variant or WT-Q1077. We previously reported that incubation with the antiarrhythmic drug mexiletine “rescued” expression deficiencies in the Brugada syndrome. Cells expressing S524Y/Q1077 and H558R/Q1077 were incubated for 48 h with or without mexiletine (500 μM), followed by drug washout before electrophysiological assessment. Mexiletine significantly increased current density for both S524Y/Q1077 and H558R/Q1077 compared with untreated cells, restoring current density to levels comparable to WT-Q1077. Flow cytometry using a FLAG-tagged channel demonstrated that mexiletine-mediated rescue was associated with increased cell-surface expression. The magnitude of the expression defects caused by H558R and S524Y in the Q1077 splice background is similar to that observed with arrhythmia-associated SCN5A mutations, and we show for the first time that the defects for both polymorphisms can be rescued with mexiletine. Although it is unknown whether they result in heightened arrhythmia susceptibility in patients homozygous for the minor allele, our result may have implications for therapy for mutations with loss-of-function phenotypes modified by these common polymorphisms. Full article
(This article belongs to the Special Issue Advances in Ion Channel Biology: From Molecular Mechanisms to Therapeutic Targets)
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