CLCA1 and TMEM16A: the link towards a potential cure for airway diseases

Expert Rev Respir Med. 2015 Oct;9(5):503-6. doi: 10.1586/17476348.2015.1081064. Epub 2015 Aug 20.

Abstract

The hallmark traits of chronic obstructive airway diseases are inflammation, airway constriction due to hyperreactivity and mucus overproduction. The current common treatments for asthma and chronic obstructive pulmonary disease target the first two traits with none currently targeting mucus overproduction. The main source of obstructive mucus production is mucus cell metaplasia (MCM), the transdifferentiation of airway epithelial cells into mucus-producing goblet cells, in the small airways. Our current understanding of MCM is profusely incomplete. Few of the molecular players involved in driving MCM in humans have been identified and for many of those that have, their functions and mechanisms are unknown. This fact has limited the development of therapeutics that target mucus overproduction by inhibiting MCM. Current work in the field is aiming to change that.

Keywords: CLCA1; COPD; TMEM16A; asthma; calcium-activated chloride channel; mucus overproduction.

Publication types

  • Editorial
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Anoctamin-1
  • Asthma / genetics
  • Asthma / physiopathology*
  • Cell Transdifferentiation / genetics
  • Chloride Channels / genetics*
  • Epithelial Cells / physiology
  • Humans
  • Mucus / physiology*
  • Neoplasm Proteins / genetics*
  • Pulmonary Disease, Chronic Obstructive / genetics
  • Pulmonary Disease, Chronic Obstructive / physiopathology*
  • Respiratory Mucosa / physiopathology*

Substances

  • ANO1 protein, human
  • Anoctamin-1
  • CLCA1 protein, human
  • Chloride Channels
  • Neoplasm Proteins