|
| Object of study | Model | Molecular mechanism | Effect | Ref |
|
| Correlation of CFTR mutations and COPD | Subjects including 20 patients with asthma, 19 with DB, and 12 with COPD | CFTR gene mutations | The hyperactive M470 allele was more frequent in COPD patients | [36] |
| Impact of ENaC on CFTR function | C57BL/6 and BALB/c mice overexpressing the beta-ENaC subunit | Overexpressing ENaC impaired CFTR function | Dysfunction of CFTR contributed to the onset and severity of COPD | [37] |
| Impact of cigarette smoke on CFTR function | Current and former smokers with or without COPD | Cigarette smoke induced CFTR dysfunction and correlated with COPD disease phenotype | Cigarette smoke induced the acquired CFTR dysfunction and contributes to COPD pathogenesis | [20] |
| CFTR in COPD pathogenesis | GOLD 0/4 patients and HBECs | Cigarette smoke reduced the expression of CFTR protein and reduced airway surface liquid height | Cigarette smoke induced CFTR dysfunction and correlated with COPD disease phenotype | [31] |
| ENaC and CFTR in COPD pathogenesis | ATI cells and ATII cells in distal lung tissues | Augmentation of ENaC induced CFTR dysfunction and impaired lung function | ENaC and CFTR-mediated chloride channel are biomarkers and potent druggable targets of COPD | [38] |
| CFTR-mediated chloride channel in COPD | Healthy and COPD smokers | CFTR-mediated chloride channel detected by β-adrenergic sweat rate | CFTR-mediated chloride channel was significantly reduced in COPD smokers as detected by β-adrenergic sweat rate, which was associated with COPD severity and clinical symptoms of COPD | [39] |
| Cigarette smoke-impaired CFTR function | Cigarette smokers and patients with COPD | Cigarette smoke induced CFTR dysfunction by reducing CFTR mRNA, accelerating degradation, and altering channel gating | Acquired CFTR induced by cigarette smoke contributed to COPD with a clinical phenotype similar to mild CF | [23] |
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