• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Expert opinion on therapeutic targets >The epithelial sodium channel (ENaC) as a therapeutic target for cystic fibrosis lung disease
【24h】

The epithelial sodium channel (ENaC) as a therapeutic target for cystic fibrosis lung disease

机译：上皮钠通道（ENAC）作为囊性纤维化肺病的治疗靶标

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Introduction: Cystic fibrosis is an autosomal recessive disorder caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene that codes for the CFTR anion channel. In the absence of functional CFTR, the epithelial Na+ channel is also dysregulated. Airway surface liquid (ASL) hydration is maintained by a balance between epithelial sodium channel (ENaC)-led Na+ absorption and CFTR-dependent anion secretion. This finely tuned homeostatic mechanism is required to maintain sufficient airway hydration to permit the efficient mucus clearance necessary for a sterile lung environment. In CF airways, the lack of CFTR and increased ENaC activity lead to ASL/mucus dehydration that causes mucus obstruction, neutrophilic infiltration, and chronic bacterial infection. Rehydration of ASL/mucus in CF airways can be achieved by inhibiting Na+ absorption with pharmacological inhibitors of ENaC. Areas covered: In this review, we discuss ENaC structure and function and its role in CF lung disease and focus on ENaC inhibition as a potential therapeutic target to rehydrate CF mucus. We also discuss the failure of the first generation of pharmacological inhibitors of ENaC and recent alternate strategies to attenuate ENaC activity in the CF lung. Expert opinion: ENaC is an attractive therapeutic target to rehydrate CF ASL that may serve as a monotherapy or function in parallel with other treatments. Given the increased number of strategies being employed to inhibit ENaC, this is an exciting and optimistic time to be in this field.
机译：介绍：囊性纤维化是由囊性纤维化跨膜电导调节剂（CFTR）基因的突变引起的常染色体隐性疾病，该基因是CFTR阴离子通道的代码。在没有功能性CFTR的情况下，上皮NA +通道也具有吸诵。气道表面液体（ASL）水合由上皮钠通道（ENAC）-LED NA +吸收和CFTR依赖性阴离子分泌之间的平衡保持。这种精细调整的稳态机制需要保持足够的气道水合，以允许无菌肺环境所需的有效粘液清除。在CF Airways中，缺乏CFTR和enac活性增加导致ASL /粘液脱水，导致粘液梗阻，中性培养性浸润和慢性细菌感染。通过抑制ENAC的药理学抑制剂，可以通过抑制Na +吸收来实现CF气道中ASL /粘液的再水化。所涵盖的地区：在本综述中，我们讨论恩克结构和功能及其在CF肺病中的作用，并专注于enac抑制作为再水化CF粘液的潜在治疗靶标。我们还讨论了ENAC第一代和最近的交替策略的第一代药理抑制剂的失败，以减弱CF肺中的enac活性。专家意见：ENAC是一种有吸引力的治疗靶标，可以补充CF AS1，其可以用作与其他治疗平行的单疗法或功能。鉴于禁止禁止enac的策略数量增加，这是在这一领域的令人兴奋和乐观的时间。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号