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The Role of Ion Channels in Health and Disease
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The Role of Ion Channels in Health and Disease

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: 20 August 2026 | Viewed by 2947

Editor

Prof. Dr. Joohyun Nam

E-Mail Website
Guest Editor
Department of Physiology, Dongguk University College of Medicine, Gyeongju 38066, Republic of Korea
Interests: ion channels & channelopathy; electrophysiology; atopic dermatitis & allergic inflammation; itch (pruritus) & pain (nociception) sensation; neuroimmunology; skin physiology & aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to this Special Issue of the International Journal of Molecular Sciences on "The Role of Ion Channels in Health and Disease". Ion channels play critical roles in numerous physiological processes, and their dysfunction is implicated in a wide spectrum of diseases. This Special Issue aims to provide a comprehensive overview of the molecular mechanisms underlying disease development related to ion channels, as well as their potential as therapeutic targets. We welcome submissions across various disciplines, including molecular biology, electrophysiology, and genomics, as long as they pertain to ion channel research. In this Special Issue, original research articles and reviews are welcome.

We look forward to hearing from you.

Prof. Dr. Joohyun Nam
Guest Editor

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 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. 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.

Keywords

  • ion channel
  • molecular mechanisms
  • channelopathies
  • drug discovery
  • electrophysiology

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Published Papers (2 papers)

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Research

18 pages, 5557 KB  
Article
Super-Resolution 3D Imaging Reveals Disarray of Dyadic Calcium Ion Channels in Failing Hearts Expressing Low Thyroid Hormone Function
by Atieh Ashkezari, Megha Schmalzle, Amanda Charest, Sanketh Kumar, Riddhi Modi, Nicholas Nasta, Andrea Bertolini, Alessandro Saba, Paolo Cifani, Youhua Zhang, A. Martin Gerdes, Randy F. Stout and Kaie Ojamaa
Int. J. Mol. Sci. 2026, 27(12), 5601; https://doi.org/10.3390/ijms27125601 - 21 Jun 2026
Viewed by 315
Abstract
Ventricular remodeling occurring in heart failure (HF) involves structural disarray of the sarcolemma T-tubule (TT)–sarcoplasmic reticulum (SR) dyad junctions, thereby disrupting the close apposition of L-type Ca2+ channels (CaV1.2) with ryanodine receptors (RyR2) that trigger SR Ca2+ release and [...] Read more.
Ventricular remodeling occurring in heart failure (HF) involves structural disarray of the sarcolemma T-tubule (TT)–sarcoplasmic reticulum (SR) dyad junctions, thereby disrupting the close apposition of L-type Ca2+ channels (CaV1.2) with ryanodine receptors (RyR2) that trigger SR Ca2+ release and myofilament contraction. In a rat ischemic heart failure model expressing low thyroid hormone (TH) function, we used 3D stochastic optical reconstruction microscopy (STORM) to image RyR2 clusters with CaV1.2 channels, and the associated protein junctophilin-2 (Jph2). We tested whether treatment with T3, the biologically active form of TH, throughout progression of the disease would preserve T-tubule structure and dyadic ion channel organization. Confocal microscopy of isolated cardiomyocytes (CMs) stained with ANEPPS membrane dye showed significantly decreased TT density in diseased CMs while T3 treatment attenuated TT disorganization. 3D STORM images of dyadic ion channels labeled with fluorescent-tagged antibodies to RyR-Dylight550, Jph-CF647 and CaV1.2/IgG-Dylight488 were captured. A density-based algorithm defined RyR2 clusters, and a 400 nm spherical 3D volume of interest around each RyR2 cluster’s centroid determined the number of CaV1.2 and Jph2 localizations associated with each RyR2 cluster. Analysis revealed significant reduction in RyR2 cluster size and number with reduced co-localized Jph2 in failing CMs. T3 treatment increased RyR2 cluster numbers and cluster volumes albeit non-significantly, with increased co-clustering of Jph2. The number of CaV1.2 co-localized with RyR2 clusters trended lower in the failing CMs. These results support maintaining TH homeostasis in optimizing the nanoscale organization of Ca2+ ion channels in triggering Ca2+ release and myofibrillar contraction in patients with heart disease. Full article
(This article belongs to the Special Issue The Role of Ion Channels in Health and Disease)
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16 pages, 2088 KB  
Article
Chronic Histamine Exposure Promotes Melanogenesis via ORAI1-STIM1-Mediated Calcium Signaling Remodeling
by Nhung Thi Hong Van, Hong Thi Lam Phan, Minh Tuan Nguyen, Woo Kyung Kim, Hyun Jong Kim and Joo Hyun Nam
Int. J. Mol. Sci. 2026, 27(4), 2055; https://doi.org/10.3390/ijms27042055 - 22 Feb 2026
Viewed by 2060
Abstract
Post-inflammatory hyperpigmentation (PIH) is a common pigmentary disorder characterized by excessive melanin production following skin inflammation. Histamine, a key inflammatory mediator, is known to stimulate melanogenesis via H2 receptors; however, the underlying calcium (Ca2+) signaling mechanisms remain largely unexplored. In [...] Read more.
Post-inflammatory hyperpigmentation (PIH) is a common pigmentary disorder characterized by excessive melanin production following skin inflammation. Histamine, a key inflammatory mediator, is known to stimulate melanogenesis via H2 receptors; however, the underlying calcium (Ca2+) signaling mechanisms remain largely unexplored. In this study, we investigated the role of the ORAI1-STIM1 complex in histamine-induced melanogenesis using B16F10 melanoma cells and normal human epidermal melanocytes (NHEMs). Histamine (10–30 μM) significantly increased melanin content (2.5–2.8-fold), an effect specifically abolished by the H2 antagonist famotidine. Notably, while acute histamine application failed to trigger immediate Ca2+ influx, chronic exposure significantly enhanced store-operated Ca2+ entry (SOCE) capacity by approximately 2.8-fold, providing evidence for a functional remodeling of the Ca2+ signaling machinery. Histamine-induced melanogenesis was significantly suppressed by intracellular Ca2+ chelation, pharmacological inhibition of ORAI1 (BTP-2 or Synta-66), and siRNA-mediated silencing of ORAI1 or STIM1, but not ORAI2, ORAI3, or STIM2. Our findings demonstrate that chronic histamine exposure drives hyperpigmentation through ORAI1-STIM1-mediated SOCE remodeling, establishing this complex as a promising therapeutic target for the treatment of PIH and related inflammatory pigmentary disorders. Full article
(This article belongs to the Special Issue The Role of Ion Channels in Health and Disease)
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