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Biomedicines
Special Issues
Novel Insight into Ion Channel and Ion-Related Signaling
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Novel Insight into Ion Channel and Ion-Related Signaling

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 10179

Special Issue Editor

Dr. Jinhong Wie

E-Mail Website
Guest Editor
Department of Physiology, Konkuk University School of Medicine, Chungju, Republic of Korea
Interests: organelle ion channel; Ca2+ signaling; drug development

Special Issue Information

Dear Colleagues,

Ions are the central balance point of the body. Ion channels are responsible for regulating the ion concentration within cells to maintain homeostasis in our body.

Because ion-related signals generated when ions pass through ion channels can be used as indicators to detect cell signaling processes during cell communication and regulation, ion channels can be used as essential targets for the development of treatments for various diseases.

In recent years, various studies have revealed the importance of ion channels and ion-related signals, yielding new insights into the function and regulation of ion channels.

This Special Issue aims to highlight cutting-edge discoveries in ion channel physiology and ion-related signaling, and introduces the latest research and advances in the field.

This Issue will provide researchers with new insights into the mechanisms of ion channel regulation and ion-related signaling.

These articles cover a wide range of topics, including new perspectives on ion channel regulation and signaling, the cellular processes of ion channels, and the development of new therapies targeting ion channels.

This Special Issue provides a comprehensive overview of the current state of research and enriches future research phases in this important field.

Dr. Jinhong Wie
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 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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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 channel
  • intracellular signaling
  • drug development
  • neurodegeneration
  • Ca2+ signaling
  • lysosomal storage disease
  • epigenetics
  • organelle ion channel
  • rare disease

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Published Papers (4 papers)

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Research

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16 pages, 2515 KiB  
Article
Identification of Novel Targeting Sites of Calcineurin and CaMKII in Human CaV3.2 T-Type Calcium Channel
by Yu-Wang Chang, Yong-Cyuan Chen and Chien-Chang Chen
Biomedicines 2023, 11(11), 2891; https://doi.org/10.3390/biomedicines11112891 - 25 Oct 2023
Viewed by 1731
Abstract
The Cav3.2 T-type calcium channel is implicated in various pathological conditions, including cardiac hypertrophy, epilepsy, autism, and chronic pain. Phosphorylation of Cav3.2 by multiple kinases plays a pivotal role in regulating its calcium channel function. The calcium/calmodulin-dependent serine/threonine phosphatase, calcineurin, interacts physically with [...] Read more.
The Cav3.2 T-type calcium channel is implicated in various pathological conditions, including cardiac hypertrophy, epilepsy, autism, and chronic pain. Phosphorylation of Cav3.2 by multiple kinases plays a pivotal role in regulating its calcium channel function. The calcium/calmodulin-dependent serine/threonine phosphatase, calcineurin, interacts physically with Cav3.2 and modulates its activity. However, it remains unclear whether calcineurin dephosphorylates Cav3.2, the specific spatial regions on Cav3.2 involved, and the extent of the quantitative impact. In this study, we elucidated the serine/threonine residues on Cav3.2 targeted by calcineurin using quantitative mass spectrometry. We identified six serine residues in the N-terminus, II–III loop, and C-terminus of Cav3.2 that were dephosphorylated by calcineurin. Notably, a higher level of dephosphorylation was observed in the Cav3.2 C-terminus, where calcineurin binds to this channel. Additionally, a previously known CaMKII-phosphorylated site, S1198, was found to be dephosphorylated by calcineurin. Furthermore, we also discovered that a novel CaMKII-phosphorylated site, S2137, underwent dephosphorylation by calcineurin. In CAD cells, a mouse central nervous system cell line, membrane depolarization led to an increase in the phosphorylation of endogenous Cav3.2 at S2137. Mutation of S2137 affected the calcium channel function of Cav3.2. Our findings advance the understanding of Cav3.2 regulation not only through kinase phosphorylation but also via calcineurin phosphatase dephosphorylation. Full article
(This article belongs to the Special Issue Novel Insight into Ion Channel and Ion-Related Signaling)
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Review

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22 pages, 3120 KiB  
Review
ClC-1 Chloride Channel: Inputs on the Structure–Function Relationship of Myotonia Congenita-Causing Mutations
by Oscar Brenes, Michael Pusch and Fernando Morales
Biomedicines 2023, 11(10), 2622; https://doi.org/10.3390/biomedicines11102622 - 24 Sep 2023
Cited by 3 | Viewed by 3335
Abstract
Myotonia congenita is a hereditary muscle disease mainly characterized by muscle hyperexcitability, which leads to a sustained burst of discharges that correlates with the magnitude and duration of involuntary aftercontractions, muscle stiffness, and hypertrophy. Mutations in the chloride voltage-gated channel 1 (CLCN1 [...] Read more.
Myotonia congenita is a hereditary muscle disease mainly characterized by muscle hyperexcitability, which leads to a sustained burst of discharges that correlates with the magnitude and duration of involuntary aftercontractions, muscle stiffness, and hypertrophy. Mutations in the chloride voltage-gated channel 1 (CLCN1) gene that encodes the skeletal muscle chloride channel (ClC-1) are responsible for this disease, which is commonly known as myotonic chloride channelopathy. The biophysical properties of the mutated channel have been explored and analyzed through in vitro approaches, providing important clues to the general function/dysfunction of the wild-type and mutated channels. After an exhaustive search for CLCN1 mutations, we report in this review more than 350 different mutations identified in the literature. We start discussing the physiological role of the ClC-1 channel in skeletal muscle functioning. Then, using the reported functional effects of the naturally occurring mutations, we describe the biophysical and structural characteristics of the ClC-1 channel to update the knowledge of the function of each of the ClC-1 helices, and finally, we attempt to point out some patterns regarding the effects of mutations in the different helices and loops of the protein. Full article
(This article belongs to the Special Issue Novel Insight into Ion Channel and Ion-Related Signaling)
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23 pages, 931 KiB  
Review
Signaling Roleplay between Ion Channels during Mammalian Sperm Capacitation
by Filip Benko, Dana Urminská, Michal Ďuračka and Eva Tvrdá
Biomedicines 2023, 11(9), 2519; https://doi.org/10.3390/biomedicines11092519 - 12 Sep 2023
Cited by 4 | Viewed by 2548
Abstract
In order to accomplish their primary goal, mammalian spermatozoa must undergo a series of physiological, biochemical, and functional changes crucial for the acquisition of fertilization ability. Spermatozoa are highly polarized cells, which must swiftly respond to ionic changes on their passage through the [...] Read more.
In order to accomplish their primary goal, mammalian spermatozoa must undergo a series of physiological, biochemical, and functional changes crucial for the acquisition of fertilization ability. Spermatozoa are highly polarized cells, which must swiftly respond to ionic changes on their passage through the female reproductive tract, and which are necessary for male gametes to acquire their functional competence. This review summarizes the current knowledge about specific ion channels and transporters located in the mammalian sperm plasma membrane, which are intricately involved in the initiation of changes within the ionic milieu of the sperm cell, leading to variations in the sperm membrane potential, membrane depolarization and hyperpolarization, changes in sperm motility and capacitation to further lead to the acrosome reaction and sperm–egg fusion. We also discuss the functionality of selected ion channels in male reproductive health and/or disease since these may become promising targets for clinical management of infertility in the future. Full article
(This article belongs to the Special Issue Novel Insight into Ion Channel and Ion-Related Signaling)
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Other

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8 pages, 534 KiB  
Commentary
Activation of σ1-Receptors by R-Ketamine May Enhance the Antidepressant Effect of S-Ketamine
by Hans O. Kalkman
Biomedicines 2023, 11(10), 2664; https://doi.org/10.3390/biomedicines11102664 - 28 Sep 2023
Cited by 4 | Viewed by 1885
Abstract
Ketamine is a racemic mixture composed of two enantiomers, S-ketamine and R-ketamine. In preclinical studies, both enantiomers have exhibited antidepressant effects, but these effects are attributed to distinct pharmacological activities. The S-enantiomer acts as an NMDA-channel blocker and as an opioid μ-receptor agonist, [...] Read more.
Ketamine is a racemic mixture composed of two enantiomers, S-ketamine and R-ketamine. In preclinical studies, both enantiomers have exhibited antidepressant effects, but these effects are attributed to distinct pharmacological activities. The S-enantiomer acts as an NMDA-channel blocker and as an opioid μ-receptor agonist, whereas the R-enantiomer binds to σ1-receptors and is believed to act as an agonist. As racemate, ketamine potentially triggers four biochemical pathways involving the AGC-kinases, PKA, Akt (PKB), PKC and RSK that ultimately lead to inhibitory phosphorylation of GSK3β in microglia. In patients with major depressive disorder, S-ketamine administered as a nasal spray has shown clear antidepressant activity. However, when compared to intravenously infused racemic ketamine, the response rate, duration of action and anti-suicidal activity of S-ketamine appear to be less pronounced. The σ1-protein interacts with μ-opioid and TrkB-receptors, whereas in preclinical experiments σ1-agonists reduce μ-receptor desensitization and improve TrkB signal transduction. TrkB activation occurs as a response to NMDA blockade. So, the σ1-activity of R-ketamine may not only enhance two pathways via which S-ketamine produces an antidepressant response, but it furthermore provides an antidepressant activity in its own right. These two factors could explain the apparently superior antidepressant effect observed with racemic ketamine compared to S-ketamine alone. Full article
(This article belongs to the Special Issue Novel Insight into Ion Channel and Ion-Related Signaling)
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