哮喘是一种常见的呼吸系统疾病,具有多方面的病理机制,对治疗发展提出挑战。SLC(溶质载体)基因家族,包含不同的膜转运蛋白,通过促进溶质穿过生物膜的运动,在各种人类疾病中起着关键作用。这些溶质包括离子,糖,糖氨基酸,神经递质,和毒品。这些离子通道的突变与许多疾病有关,强调SLC基因家族在生理过程中的重要性。其中,SLC26A4基因编码pendrin,参与氯离子跨膜转运的阴离子交换蛋白,碘化物,和碳酸氢盐。SLC26A4突变与Pendred综合征相关SLC26A4表达升高与气道炎症有关,高反应性,和哮喘的粘液产生。这里,我们回顾了SLC基因家族成员对底物转运和疾病关联机制的新见解,特别强调SLC26A4。我们探索诱导SLC26A4表达的触发因素及其对肺部疾病发病机理的贡献,特别是哮喘。我们总结了SLC26A4的抑制剂,这些抑制剂在治疗不同表型的疾病中显示出希望。虽然SLC26A4抑制剂为哮喘提供了潜在的治疗方法,进一步的研究对于明确它们在哮喘发病机制中的作用以及开发针对该蛋白的有效治疗策略至关重要.
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.