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Solute Carrier Family 26 Member 4 (SLC26A4), A Potential Therapeutic Target for Asthma.
Guntupalli, Vineeta; Wan, Rongjun; Liu, Liyuan; Gu, Wenjing; Xie, Shaobing; Gao, Peisong.
Affiliation
  • Guntupalli V; Division of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
  • Wan R; Division of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
  • Liu L; Department of Respiratory and Critical Care Medicine, Xiangya Hospital, Central South University, Changsha 410008, China.
  • Gu W; Division of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
  • Xie S; Division of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
  • Gao P; Department of Respiratory Medicine, Children's Hospital of Soochow University, Suzhou 215000, China.
Article in En | MEDLINE | ID: mdl-39100210
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.
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: J Respir Biol Transl Med Year: 2024 Type: Article Affiliation country: United States

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: J Respir Biol Transl Med Year: 2024 Type: Article Affiliation country: United States