ArticleJournal of respiratory biology and translational medicine2024
Solute Carrier Family 26 Member 4 (SLC26A4), A Potential Therapeutic Target for Asthma.
Article in Journal of respiratory biology and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Genomic characterization and pathogenicity validation of Mycoplasma ovipneumoniae strains from diseased sheep: insights into potential pathogenic mechanisms of GSWW364.Veterinary research · 2026Article
- The role of CFTR in spermatogenesis and sperm quality.Nature reviews. Urology · 2026Review
- Machine Learning-Based Validation of LDHC and SLC35G2 Methylation as Epigenetic Biomarkers for Food Allergy.Biomedicines · 2025Article
- Genetic mutations in lymphocytic variant of hypereosinophilic syndrome: study of five siblings.Frontiers in medicine · 2025Article
- Ion Channels in the Immune Response of Asthma.Journal of respiratory biology and translational medicine · 2024Article
- Progress and Gaps in Respiratory Disease Research and Treatment: Highlights of the IRM 2024 in Shanghai.Journal of respiratory biology and translational medicine · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Asthma is a prevalent respiratory condition with multifaceted pathomechanisms, presenting challenges for therapeutic development. The SLC (Solute Carrier) gene family, encompassing diverse membrane transport proteins, plays pivotal roles in various human diseases by facilitating solute movement across biological membranes. These solutes include ions, sugars, amino acids, neurotransmitters, and drugs. Mutations in these ion channels have been associated with numerous disorders, underscoring the significance of SLC gene families in physiological processes. Among these, the SLC26A4 gene encodes pendrin, an anion exchange protein involved in transmembrane transport of chloride, iodide, and bicarbonate. Mutations in SLC26A4 are associated with Pendred syndrome. Elevated SLC26A4 expression has been linked to airway inflammation, hyperreactivity, and mucus production in asthma. Here, we review novel insights from SLC gene family members into the mechanisms of substrate transport and disease associations, with specific emphasis on SLC26A4. We explore triggers inducing SLC26A4 expression and its contributions to the pathogenesis of pulmonary diseases, particularly asthma. We summarize the inhibitors of SLC26A4 that have shown promise in the treatment of different phenotypes of diseases. While SLC26A4 inhibitors present potential treatments for asthma, further research is imperative to delineate their precise role in asthma pathogenesis and develop efficacious therapeutic strategies targeting this protein.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.