| Literature DB >> 29339516 |
Benjamin M Smith1,2, Hussein Traboulsi2, John H M Austin3, Ani Manichaikul4, Eric A Hoffman5,6,7, Eugene R Bleecker8, Wellington V Cardoso9, Christopher Cooper10, David J Couper11, Stephen M Dashnaw3, Jia Guo12, MeiLan K Han13, Nadia N Hansel14, Emlyn W Hughes15, David R Jacobs16, Richard E Kanner17, Joel D Kaufman18, Eric Kleerup10, Ching-Long Lin19, Kiang Liu20, Christian M Lo Cascio9, Fernando J Martinez21, Jennifer N Nguyen4, Martin R Prince3, Stephen Rennard22, Stephen S Rich4, Leora Simon2, Yanping Sun9, Karol E Watson10, Prescott G Woodruff23, Carolyn J Baglole2, R Graham Barr9,24.
Abstract
Susceptibility to chronic obstructive pulmonary disease (COPD) beyond cigarette smoking is incompletely understood, although several genetic variants associated with COPD are known to regulate airway branch development. We demonstrate that in vivo central airway branch variants are present in 26.5% of the general population, are unchanged over 10 y, and exhibit strong familial aggregation. The most common airway branch variant is associated with COPD in two cohorts (n = 5,054), with greater central airway bifurcation density, and with emphysema throughout the lung. The second most common airway branch variant is associated with COPD among smokers, with narrower airway lumens in all lobes, and with genetic polymorphisms within the FGF10 gene. We conclude that central airway branch variation, readily detected by computed tomography, is a biomarker of widely altered lung structure with a genetic basis and represents a COPD susceptibility factor.Entities:
Keywords: airway branching; chronic obstructive pulmonary disease; computed tomography; fibroblast growth factor
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Year: 2018 PMID： 29339516 PMCID： PMC5798356 DOI： 10.1073/pnas.1715564115
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205