Extract
Bronchiectasis is a heterogeneous chronic structural lung disease in which four canonical elements of a vicious circle, i.e. recurrent airway infections, impaired mucociliary clearance, chronic airway inflammation and irreversible airway dilatation, have been implicated [1, 2]. Unravelling the underlying causes of bronchiectasis, which can only be ascertained in approximately 50% of patients despite exhaustive diagnostic efforts [3], is clinically relevant for optimising therapeutic interventions by targeting the core pathophysiology. There are a number of primary underlying causes, for instance, primary ciliary dyskinesia, which affects the motile cilia, cystic fibrosis, and congenital malformation. Several studies have indicated a role of genetic mutations in bronchiectasis [4–6], evidenced by the possible link with the clinical phenotypes and disease severity. These studies also suffered from a limited capacity of thoroughly identifying the genes broadly representative of pathophysiology.
Abstract
Transcriptomic profiling helps to unveil the pathophysiology of bronchiectasis https://bit.ly/3C1B6JA
Footnotes
Author contributions: W-J. Guan, P-C. Hu and M.A. Martinez-Garcia drafted and critically reviewed the manuscript. All authors have approved for the final submission.
Conflict of interest: All authors declare no potential conflict of interest related to this paper
Support statement: National Natural Science Foundation – Outstanding Youth Fund (number 82222001), National Natural Science Foundation (number 81870003), Guangdong Science and Technology Foundation (number 2019B030316028) and Zhongnanshan Medical Foundation of Guangdong Province (number ZNSA-2020013) (to W-J. Guan). M.A. Martinez-Garcia has no source of funding related to this paper. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received September 4, 2022.
- Accepted September 16, 2022.
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