Special Issue "Chloride Channels and Transporters in Health and Disease"

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: 30 April 2023 | Viewed by 2506

Special Issue Editors

1. U.O.C. Genetica Medica, IRCCS Istituto Giannina Gaslini, 16147 Genova, Italy
2. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), Università degli Studi di Genova, 16132 Genova, Italy
Interests: cystic fibrosis; epithelial physiology; airway physiology; TMEM16 genes; ion channel; phospholipid scramblases; in vitro models; neurodevelopmental disorders; induced pluripotent stem cells; brain organoids; therapeutic development; high content imaging; high throughput screening
Special Issues, Collections and Topics in MDPI journals
DiNOGMI, Università di Genova, U.O.C. Genetica Medica, IRCSS Istituto Giannina Gaslini, Via Gerolamo Gaslini 5, 16147 - Genova , Italy
Interests: Rare genetic diseases; neurodevelopmental disorders; cystic fibrosis; epithelial physiology; ion channels; metabotropic receptors; phospholipid scramblases; in vitro models; induced pluripotent stem cells; neuronal culture; brain organoids

Special Issue Information

Dear Colleagues,

Chloride is the most abundant anion in animal cells and chloride channels have fundamental role in physiology and disease. Chloride channels are indeed involved in a variety of biological functions, including trans-epithelial fluid secretion, cell volume regulation, cellular signaling, and vesicular trafficking and acidification. Different types of chloride channels have been identified, and many of them are implicated in severe human diseases. For example, CFTR (a cAMP-dependent anion channel) and CLC-1 (a voltage-gated chloride channel), which are the first two human chloride channels that have been cloned, are involved, as causative genes, in cystic fibrosis and myotonia congenita, respectively. In the last decade, many other chloride channels, regulated by calcium (for example TMEM16A), cell volume (LRRC8) or pH (TMEM206) have been identified and are now under deeply investigation to highlight their contributions to physiology, pathogenesis and as potential therapeutic targets in genetic diseases and cancer.

This Special Issue calls for original research, reviews, and perspectives that address the current knowledge in the field of chloride channels and transporters involved in human physiology and disease.

Dr. Paolo Scudieri
Dr. Ilaria Musante
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2300 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.


  • chloride channels
  • anionic transporters
  • calcium signaling
  • volume regulation
  • pH regulation
  • intracellular channels
  • electrophysiology
  • pharmacology
  • optogenetics
  • in vitro models
  • CRISPR/Cas9

Published Papers (1 paper)

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SLC26A9 as a Potential Modifier and Therapeutic Target in Cystic Fibrosis Lung Disease
Biomolecules 2022, 12(2), 202; https://doi.org/10.3390/biom12020202 - 25 Jan 2022
Cited by 1 | Viewed by 2189
SLC26A9 belongs to the solute carrier family 26 (SLC26), which comprises membrane proteins involved in ion transport mechanisms. On the basis of different preliminary findings, including the phenotype of SlC26A9-deficient mice and its possible role as a gene modifier of the human phenotype [...] Read more.
SLC26A9 belongs to the solute carrier family 26 (SLC26), which comprises membrane proteins involved in ion transport mechanisms. On the basis of different preliminary findings, including the phenotype of SlC26A9-deficient mice and its possible role as a gene modifier of the human phenotype and treatment response, SLC26A9 has emerged as one of the most interesting alternative targets for the treatment of cystic fibrosis (CF). However, despite relevant clues, some open issues and controversies remain. The lack of specific pharmacological modulators, the elusive expression reported in the airways, and its complex relationships with CFTR and the CF phenotype prevent us from conclusively understanding the contribution of SLC26A9 in human lung physiology and its real potential as a therapeutic target in CF. In this review, we summarized the various studies dealing with SLC26A9 expression, molecular structure, and function as an anion channel or transporter; its interaction and functional relationships with CFTR; and its role as a gene modifier and tried to reconcile them in order to highlight the current understanding and the gap in knowledge regarding the contribution of SLC26A9 to human lung physiology and CF disease and treatment. Full article
(This article belongs to the Special Issue Chloride Channels and Transporters in Health and Disease)
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