Literature DB >> 19137504

[The genetics of chronic obstructive pulmonary disease].

U Arinir1, S Hoffjan, H Knoop, G Schultze-Werninghaus, J T Epplen, G Rohde.   

Abstract

COPD is a heterogenous disease caused by the interaction of genetic susceptibility and environmental influences. The best example to support this is tobacco smoke. Although cigarette smoking is the most important aetiological factor, only up to half of chronic smokers develop significant COPD. There are three main themes within the pathogenesis of COPD: 1) imbalance between proteases and anti-proteases, 2) oxidative stress, 3) inflammation. Disparity between levels of exogeneous oxidants, e. g., tobacco smoke, and endogeneous antioxidants leads to oxidative stress which, in turn, causes an inflammatory response involving pro-inflammatory mediators. The activated inflammatory cells release further proteases and oxidants, leading to chronic inflammation and irreversible destruction of connective tissue in the lung. Individual genetic variations influence these processes in many ways. This article summarises the results of recent candidate gene studies for COPD.

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Year:  2009        PMID: 19137504     DOI: 10.1055/s-0028-1100824

Source DB:  PubMed          Journal:  Pneumologie        ISSN: 0934-8387


  1 in total

1.  A Functional Variant rs6435156C > T in BMPR2 is Associated With Increased Risk of Chronic Obstructive Pulmonary Disease (COPD) in Southern Chinese Population.

Authors:  Jian Wang; Chenting Zhang; Zili Zhang; Zeguang Zheng; Dejun Sun; Quan Yang; Cyrus Hadadi; Defu Li; Xiaoming Xu; Mingmei Xiong; Qipeng Zhou; Meihua Guo; Yingfeng Wang; Chun Tang; Guihua Xu; Kai Yang; Nanshan Zhong; Wenju Lu
Journal:  EBioMedicine       Date:  2016-02-05       Impact factor: 8.143

  1 in total

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