Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
5.2
3.9
Journals
Biomedicines
Special Issues
The Role of Ion Channels and Transporters in Human Health...
share announcement

The Role of Ion Channels and Transporters in Human Health and Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 December 2024) | Viewed by 17949

Special Issue Editor

Dr. Teresa Soda

E-Mail Website
Guest Editor
Department of Health Science, Laboratory of Physiology and Neuropharmacology, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy
Interests: synaptic plasticity; NMDAreceptor; autism; endothelial cell; neurovascular coupling; Ca2+ signaling; nitric oxide
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The human body relies on a delicate balance of various elements, including the precise movement of ions, electrically charged atoms, or molecules, across cell membranes. This critical task requires two crucial players: ion channels and transporters. An intricate network of membrane proteins orchestrates the flow of ions, dictating their entry and exit from cells and their release or sequestration by endogenous organelles. This meticulously controlled movement underpins numerous physiological processes, forming the very foundation of human health. Ion channels act as selective pores, opening and closing in response to various stimuli like voltage changes or the presence of specific molecules. They allow specific ions, like sodium, potassium, chloride, and calcium, to pass through the membrane, generating electrical signals and enabling communication within and between cells. In addition, water channels, known as aquaporin, are pivotal to fine-tune cellular volume during osmotic challenges. On the other hand, transporters actively move ions and solutes according to or against their concentration gradient, ensuring their proper distribution and controlling their concentration within cells. This precise control is vital for maintaining homeostasis, the stable internal environment required for cellular function. Transporters also play a key role in nutrient absorption, facilitating the uptake of essential molecules from the gut into the bloodstream for distribution throughout the body. The importance of ion channels and transporters cannot be overstated. Their proper function is vital for countless physiological processes, including synaptic transmission and plasticity, muscle contraction, fluid balance, secretion, and absorption. When these proteins malfunction, it can lead to a cascade of consequences, disrupting the delicate cellular equilibrium and causing various illnesses. Therefore, understanding the intricacies of ion channels and transporters is critical for comprehending human health and disease. The following sections will explore the specific roles these proteins play in various diseases and the potential for therapeutic interventions based on this knowledge.

I am pleased to invite you to participate in this Special Issue. Experimental papers and up-to-date review articles are all welcome.

Dr. Teresa Soda
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 channels
  • transporters
  • ion pumps
  • voltage-gated channels
  • ionotropic receptors
  • TRP channels
  • store-operated channels
  • Piezo channels
  • NALCN channels
  • inositol-1,4,5-receptors
  • ryanodine receptors
  • two-pore channels
  • synaptic transmission
  • channelopathies
  • neurodegenerative disorders
  • cardiovascular disorders

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 policies can be found here.

Related Special Issue

Published Papers (8 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

16 pages, 5630 KiB  
Article
Identifying a Role for the Sodium Hydrogen Exchanger Isoform 1 in Idiopathic Pulmonary Fibrosis: A Potential Strategy to Modulate Profibrotic Pathways
by Trina T. Nguyentu, Danielle G. Vigilante, Mishika Manchanda, Meera S. Iyer, Sara Desalegne and Joseph J. Provost
Biomedicines 2025, 13(4), 959; https://doi.org/10.3390/biomedicines13040959 - 14 Apr 2025
Viewed by 357
Abstract
Background/Objectives: Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by excessive extracellular matrix (ECM) production and tissue stiffening, resulting in impaired lung function. Sodium hydrogen exchanger isoform 1 (NHE1) is a key mediator of intracellular and extracellular pH regulation, influencing [...] Read more.
Background/Objectives: Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by excessive extracellular matrix (ECM) production and tissue stiffening, resulting in impaired lung function. Sodium hydrogen exchanger isoform 1 (NHE1) is a key mediator of intracellular and extracellular pH regulation, influencing fibroblast activation, motility, and proliferative pathways. This study investigates the role of NHE1 in actin stress fiber formation, fibroblast-to-myofibroblast differentiation, and cytokine secretion in IPF progression. Methods: Fibroblasts were treated with profibrotic agonists, including transforming growth factor-beta (TGFβ), lysophosphatidic acid (LPA), and serotonin (THT), in the presence or absence of the NHE1-specific inhibitor, EIPA. Actin stress fibers were visualized using phalloidin staining, while α-smooth muscle actin (α-SMA) expression and cytokine secretion (TGFβ, IL-6, and IL-8) were quantified using immunostaining and ELISA. Intracellular pH changes were measured using BCECF-AM fluorescence. Results: Profibrotic agonists induced significant actin stress fiber formation and α-SMA expression in fibroblasts, both of which were abolished by EIPA. NHE1 activity was shown to mediate intracellular alkalization, a critical factor for fibroblast activation. Cytokine secretion, including TGFβ, IL-6, and IL-8, was enhanced by agonist treatments but reduced with NHE1 inhibition. Chronic TGFβ exposure increased intracellular pH and sustained myofibroblast differentiation, which was partially reversed by EIPA. Conclusions: NHE1 is indicated to play a novel and potential role in processes supporting profibrotic agonists driving fibroblast activation and IPF progression. Targeting NHE1 could present a potential therapeutic approach to disrupt profibrotic pathways and mitigate IPF severity. Full article
(This article belongs to the Special Issue The Role of Ion Channels and Transporters in Human Health and Diseases)
►▼ Show Figures

Figure 1

16 pages, 2587 KiB  
Article
Rescue of Mutant CFTR Channel Activity by Investigational Co-Potentiator Therapy
by Mafalda Bacalhau, Filipa C. Ferreira, Marcelo Folhadella M. F. Azevedo, Talita P. Rosa, Camilla D. Buarque and Miquéias Lopes-Pacheco
Biomedicines 2025, 13(1), 82; https://doi.org/10.3390/biomedicines13010082 - 1 Jan 2025
Cited by 1 | Viewed by 2085
Abstract
Background: The potentiator VX-770 (ivacaftor) has been approved as a monotherapy for over 95 cystic fibrosis (CF)-causing variants associated with gating/conductance defects of the CF transmembrane conductance regulator (CFTR) channel. However, despite its therapeutic success, VX-770 only partially restores CFTR activity for many [...] Read more.
Background: The potentiator VX-770 (ivacaftor) has been approved as a monotherapy for over 95 cystic fibrosis (CF)-causing variants associated with gating/conductance defects of the CF transmembrane conductance regulator (CFTR) channel. However, despite its therapeutic success, VX-770 only partially restores CFTR activity for many of these variants, indicating they may benefit from the combination of potentiators exhibiting distinct mechanisms of action (i.e., co-potentiators). We previously identified LSO-24, a hydroxy-1,2,3-triazole-based compound, as a modest potentiator of p.Arg334Trp-CFTR, a variant with a conductance defect for which no modulator therapy is currently approved. Objective/Methods: We synthesized a new set of LSO-24 structure-based compounds, screened their effects on p.Arg334Trp-CFTR activity, and assessed the additivity of hit compounds to VX-770, ABBV-974, ABBV-3067, and apigenin. After validation by electrophysiological assays, the most promising hits were also assessed in cells expressing other variants with defective gating/conductance, namely p.Pro205Ser, p.Ser549Arg, p.Gly551Asp, p.Ser945Leu, and p.Gly1349Asp. Results: We found that five compounds were able to increase p.Arg334Trp-CFTR activity with similar efficacy, but slightly greater potency promoted by LSO-150 and LSO-153 (EC50: 1.01 and 1.26 μM, respectively). These two compounds also displayed a higher rescue of p.Arg334Trp-CFTR activity in combination with VX-770, ABBV-974, and ABBV-3067, but not with apigenin. When tested in cells expressing other CFTR variants, LSO-24 and its derivative LSO-150 increased CFTR activity for the variants p.Ser549Arg, p.Gly551Asp, and p.Ser945Leu with a further effect in combination with VX-770 or ABBV-3067. No potentiator was able to rescue CFTR activity in p.Pro205Ser-expressing cells, while p.Gly1349Asp-CFTR responded to VX-770 and ABBV-3067 but not to LSO-24 or LSO-150. Conclusions: Our data suggest that these new potentiators might share a common mechanism with apigenin, which is conceivably distinct from that of VX-770 and ABBV-3067. The additive rescue of p.Arg334Trp-, p.Ser549Arg-, p.Gly551Asp-, and p.Ser945Leu-CFTR also indicates that these variants could benefit from the development of a co-potentiator therapy. Full article
(This article belongs to the Special Issue The Role of Ion Channels and Transporters in Human Health and Diseases)
►▼ Show Figures

Figure 1

16 pages, 1838 KiB  
Article
SGLT-2 Inhibitors’ and GLP-1 Receptor Agonists’ Influence on Neuronal and Glial Damage in Experimental Stroke
by Anna Murasheva, Oksana Fuks, Natalya Timkina, Arina Mikhailova, Timur Vlasov, Konstantin Samochernykh and Tatiana Karonova
Biomedicines 2024, 12(12), 2797; https://doi.org/10.3390/biomedicines12122797 - 10 Dec 2024
Viewed by 988
Abstract
Background: SGLT-2 inhibitors (SGLT-2i) and GLP-1 receptor agonists (GLP-1RA) have demonstrated nephro- and cardioprotective effects, but their neuroprotective properties, especially concerning stroke severity, and mechanisms are not unambiguous. We aimed to study the influence of SGLT-2i with different selectivity and GLP-1RA on brain [...] Read more.
Background: SGLT-2 inhibitors (SGLT-2i) and GLP-1 receptor agonists (GLP-1RA) have demonstrated nephro- and cardioprotective effects, but their neuroprotective properties, especially concerning stroke severity, and mechanisms are not unambiguous. We aimed to study the influence of SGLT-2i with different selectivity and GLP-1RA on brain damage volume and neurological status in non-diabetic and diabetic rats and to investigate the underlying mechanisms. Methods: Non-diabetic Wistar rats were divided into five groups (n = 10 each) and received empagliflozin, canagliflozin, or dulaglutide as study drugs and metformin as comparison drug. Control animals were administered 0.9% NaCl for 7 days before stroke. At 48 h after stroke, we assessed neurological deficit, neuronal and astroglial damage markers, and brain damage volume. We also modeled type 2 DM in Wistar rats using the high-fat diet+nicotinamide/streptozotocin method and established similar treatment groups. After 8 weeks, rats were subjected to stroke with further neurological deficit, neuroglial damage markers, and brain necrosis volume measurement. Results: In non-diabetic rats, all the drugs showed an infarct-limiting effect; SGLT-2i and dulaglutide were more effective than metformin. DULA improved neurological status compared with MET and SGLT-2i treatment. All the drugs decreased neurofilament light chains (NLCs) level and neuronal damage markers, but none of them decreased the glial damage marker S100BB. In DM, similarly, all the drugs had infarct-limiting effects. Neurological deficit was most pronounced in the untreated diabetic rats and was reduced by all study drugs. All the drugs reduced NLC level; dulaglutide and empagliflozin, but not canagliflozin, also decreased S100BB. None of the drugs affected neuron-specific enolase. Conclusions: SGLT-2i and GLP-1RA are neuroprotective in experimental stroke. GLP-1RA might be more effective than SGLT-2i as in non-diabetic conditions it influences both brain damage volume and neurological status. All study drugs decrease neuronal damage, while GLP-1RA and highly selective SGLT-2i EMPA, but not low-selective CANA, also have an impact on neuroglia in diabetic conditions. Full article
(This article belongs to the Special Issue The Role of Ion Channels and Transporters in Human Health and Diseases)
►▼ Show Figures

Figure 1

19 pages, 4438 KiB  
Article
The Functional Interaction of KATP and BK Channels with Aquaporin-4 in the U87 Glioblastoma Cell
by Fatima Maqoud, Laura Simone, Domenico Tricarico, Giulia Maria Camerino, Marina Antonacci and Grazia Paola Nicchia
Biomedicines 2024, 12(8), 1891; https://doi.org/10.3390/biomedicines12081891 - 19 Aug 2024
Viewed by 4173
Abstract
K+ channels do play a role in cell shape changes observed during cell proliferation and apoptosis. Research suggested that the dynamics of the aggregation of Aquaporin-4 (AQP4) into AQP4-OAP isoforms can trigger cell shape changes in malignant glioma cells. Here, we investigated [...] Read more.
K+ channels do play a role in cell shape changes observed during cell proliferation and apoptosis. Research suggested that the dynamics of the aggregation of Aquaporin-4 (AQP4) into AQP4-OAP isoforms can trigger cell shape changes in malignant glioma cells. Here, we investigated the relationship between AQP4 and some K+ channels in the malignant glioma U87 line. The U87 cells transfected with the human M1-AQP4 and M23-AQP4 isoforms were investigated for morphology, the gene expression of KCNJ8, KCNJ11, ABCC8, ABCC9, KCNMA1, and Cyclin genes by RT-PCR, recording the whole-cell K+ ion currents by patch-clamp experiments. AQP4 aggregation into OAPs increases the plasma membrane functional expression of the Kir6.2 and SUR2 subunits of the KATP channels and of the KCNMA1 of the BK channels in U87 cells leading to a large increase in inward and outward K+ ion currents. These changes were associated with changes in morphology, with a decrease in cell volume in the U87 cells and an increase in the ER density. These U87 cells accumulate in the mitotic and G2 cell cycle. The KATP channel blocker zoledronic acid reduced cell proliferation in both M23 AQP4-OAP and M1 AQP4-tetramer-transfected cells, leading to early and late apoptosis, respectively. The BK channel sustains the efflux of K+ ions associated with the M23 AQP4-OAP expression in the U87 cells, but it is downregulated in the M1 AQP4-tetramer cells. The KATP channels are effective in the M1 AQP4-tetramer and M23 AQP4-OAP cells. Zoledronic acid can be effective in targeting pathogenic M1 AQP4-tetramer cell phenotypes inhibiting KATP channels and inducing early apoptosis. Full article
(This article belongs to the Special Issue The Role of Ion Channels and Transporters in Human Health and Diseases)
►▼ Show Figures

Figure 1

13 pages, 3173 KiB  
Article
Chronic Mexiletine Administration Increases Sodium Current in Non-Diseased Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes
by Giovanna Nasilli, Arie O. Verkerk, Molly O’Reilly, Loukia Yiangou, Richard P. Davis, Simona Casini and Carol Ann Remme
Biomedicines 2024, 12(6), 1212; https://doi.org/10.3390/biomedicines12061212 - 29 May 2024
Cited by 1 | Viewed by 1857
Abstract
A sodium current (INa) reduction occurs in the setting of many acquired and inherited conditions and is associated with cardiac conduction slowing and increased arrhythmia risks. The sodium channel blocker mexiletine has been shown to restore the trafficking of mutant sodium [...] Read more.
A sodium current (INa) reduction occurs in the setting of many acquired and inherited conditions and is associated with cardiac conduction slowing and increased arrhythmia risks. The sodium channel blocker mexiletine has been shown to restore the trafficking of mutant sodium channels to the membrane. However, these studies were mostly performed in heterologous expression systems using high mexiletine concentrations. Moreover, the chronic effects on INa in a non-diseased cardiomyocyte environment remain unknown. In this paper, we investigated the chronic and acute effects of a therapeutic dose of mexiletine on INa and the action potential (AP) characteristics in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) of a healthy individual. Control hiPSC-CMs were incubated for 48 h with 10 µM mexiletine or vehicle. Following the wash-out of mexiletine, patch clamp analysis and immunocytochemistry experiments were performed. The incubation of hiPSC-CMs for 48 h with mexiletine (followed by wash-out) induced a significant increase in peak INa of ~75%, without any significant change in the voltage dependence of (in)activation. This was accompanied by a significant increase in AP upstroke velocity, without changes in other AP parameters. The immunocytochemistry experiments showed a significant increase in membrane Nav1.5 fluorescence following a 48 h incubation with mexiletine. The acute re-exposure of hiPSC-CMs to 10 µM mexiletine resulted in a small but significant increase in AP duration, without changes in AP upstroke velocity, peak INa density, or the INa voltage dependence of (in)activation. Importantly, the increase in the peak INa density and resulting AP upstroke velocity induced by chronic mexiletine incubation was not counteracted by the acute re-administration of the drug. In conclusion, the chronic administration of a clinically relevant concentration of mexiletine increases INa density in non-diseased hiPSC-CMs, likely by enhancing the membrane trafficking of sodium channels. Our findings identify mexiletine as a potential therapeutic strategy to enhance and/or restore INa and cardiac conduction. Full article
(This article belongs to the Special Issue The Role of Ion Channels and Transporters in Human Health and Diseases)
►▼ Show Figures

Figure 1

Review

Jump to: Research

29 pages, 3011 KiB  
Review
Sodium Chloride Cotransporter in Hypertension
by Annalisa Castagna, Gabriele Mango, Nicola Martinelli, Luigi Marzano, Sara Moruzzi, Simonetta Friso and Francesca Pizzolo
Biomedicines 2024, 12(11), 2580; https://doi.org/10.3390/biomedicines12112580 - 11 Nov 2024
Viewed by 2696
Abstract
The sodium chloride cotransporter (NCC) is essential for electrolyte balance, blood pressure regulation, and pathophysiology of hypertension as it mediates the reabsorption of ultrafiltered sodium in the renal distal convoluted tubule. Given its pivotal role in the maintenance of extracellular fluid volume, the [...] Read more.
The sodium chloride cotransporter (NCC) is essential for electrolyte balance, blood pressure regulation, and pathophysiology of hypertension as it mediates the reabsorption of ultrafiltered sodium in the renal distal convoluted tubule. Given its pivotal role in the maintenance of extracellular fluid volume, the NCC is regulated by a complex network of cellular pathways, which eventually results in either its phosphorylation, enhancing sodium and chloride ion absorption from urines, or dephosphorylation and ubiquitination, which conversely decrease NCC activity. Several factors could influence NCC function, including genetic alterations, hormonal stimuli, and pharmacological treatments. The NCC’s central role is also highlighted by several abnormalities resulting from genetic mutations in its gene and consequently in its structure, leading to dysregulation of blood pressure control. In the last decade, among other improvements, the acquisition of knowledge on the NCC and other renal ion channels has been favored by studies on extracellular vesicles (EVs). Dietary sodium and potassium intake are also implicated in the tuning of NCC activity. In this narrative review, we present the main cornerstones and recent evidence related to NCC control, focusing on the context of blood pressure pathophysiology, and promising new therapeutical approaches. Full article
(This article belongs to the Special Issue The Role of Ion Channels and Transporters in Human Health and Diseases)
►▼ Show Figures

Graphical abstract

34 pages, 3310 KiB  
Review
Two Signaling Modes Are Better than One: Flux-Independent Signaling by Ionotropic Glutamate Receptors Is Coming of Age
by Valentina Brunetti, Teresa Soda, Roberto Berra-Romani, Giovambattista De Sarro, Germano Guerra, Giorgia Scarpellino and Francesco Moccia
Biomedicines 2024, 12(4), 880; https://doi.org/10.3390/biomedicines12040880 - 16 Apr 2024
Cited by 5 | Viewed by 2159
Abstract
Glutamate is the major excitatory neurotransmitter in the central nervous system. Glutamatergic transmission can be mediated by ionotropic glutamate receptors (iGluRs), which mediate rapid synaptic depolarization that can be associated with Ca2+ entry and activity-dependent change in the strength of synaptic transmission, [...] Read more.
Glutamate is the major excitatory neurotransmitter in the central nervous system. Glutamatergic transmission can be mediated by ionotropic glutamate receptors (iGluRs), which mediate rapid synaptic depolarization that can be associated with Ca2+ entry and activity-dependent change in the strength of synaptic transmission, as well as by metabotropic glutamate receptors (mGluRs), which mediate slower postsynaptic responses through the recruitment of second messenger systems. A wealth of evidence reported over the last three decades has shown that this dogmatic subdivision between iGluRs and mGluRs may not reflect the actual physiological signaling mode of the iGluRs, i.e., α-amino-3-hydroxy-5-methyl-4-isoxasolepropionic acid (AMPA) receptors (AMPAR), kainate receptors (KARs), and N-methyl-D-aspartate (NMDA) receptors (NMDARs). Herein, we review the evidence available supporting the notion that the canonical iGluRs can recruit flux-independent signaling pathways not only in neurons, but also in brain astrocytes and cerebrovascular endothelial cells. Understanding the signaling versatility of iGluRs can exert a profound impact on our understanding of glutamatergic synapses. Furthermore, it may shed light on novel neuroprotective strategies against brain disorders. Full article
(This article belongs to the Special Issue The Role of Ion Channels and Transporters in Human Health and Diseases)
►▼ Show Figures

Graphical abstract

16 pages, 2385 KiB  
Review
Transporters, Ion Channels, and Junctional Proteins in Choroid Plexus Epithelial Cells
by Masaki Ueno, Yoichi Chiba, Ryuta Murakami, Yumi Miyai, Koichi Matsumoto, Keiji Wakamatsu, Toshitaka Nakagawa, Genta Takebayashi, Naoya Uemura, Ken Yanase and Yuichi Ogino
Biomedicines 2024, 12(4), 708; https://doi.org/10.3390/biomedicines12040708 - 22 Mar 2024
Cited by 3 | Viewed by 2343
Abstract
The choroid plexus (CP) plays significant roles in secreting cerebrospinal fluid (CSF) and forming circadian rhythms. A monolayer of epithelial cells with tight and adherens junctions of CP forms the blood–CSF barrier to control the movement of substances between the blood and ventricles, [...] Read more.
The choroid plexus (CP) plays significant roles in secreting cerebrospinal fluid (CSF) and forming circadian rhythms. A monolayer of epithelial cells with tight and adherens junctions of CP forms the blood–CSF barrier to control the movement of substances between the blood and ventricles, as microvessels in the stroma of CP have fenestrations in endothelial cells. CP epithelial cells are equipped with several kinds of transporters and ion channels to transport nutrient substances and secrete CSF. In addition, junctional components also contribute to CSF production as well as blood–CSF barrier formation. However, it remains unclear how junctional components as well as transporters and ion channels contribute to the pathogenesis of neurodegenerative disorders. In this manuscript, recent findings regarding the distribution and significance of transporters, ion channels, and junctional proteins in CP epithelial cells are introduced, and how changes in expression of their epithelial proteins contribute to the pathophysiology of brain disorders are reviewed. Full article
(This article belongs to the Special Issue The Role of Ion Channels and Transporters in Human Health and Diseases)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-8
Back to TopTop