Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 295, Issue 2, Pages L240-L263Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.90203.2008
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Funding
- Howard Hughes Medical Institute Funding Source: Medline
- NCRR NIH HHS [RR-13438] Funding Source: Medline
- NHLBI NIH HHS [HL-07638, HL-51670] Funding Source: Medline
- NIDCR NIH HHS [R01 DE014390] Funding Source: Medline
- NIDDK NIH HHS [P30 DK054759, R37 DK047967, DK-54759] Funding Source: Medline
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Airway disease currently causes most of the morbidity and mortality in patients with cystic fibrosis (CF). However, understanding the pathogenesis of CF lung disease and developing novel therapeutic strategies have been hampered by the limitations of current models. Although the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) has been targeted in mice, CF mice fail to develop lung or pancreatic disease like that in humans. In many respects, the anatomy, biochemistry, physiology, size, and genetics of pigs resemble those of humans. Thus pigs with a targeted CFTR gene might provide a good model for CF. Here, we review aspects of porcine airways and lung that are relevant to CF.
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