It is not just tobacco that increases the risk of developing chronic obstructive pulmonary disease. 6 genes act independently.
In addition to tobacco and pollution, genes increase the risk of chronic obstructive pulmonary disease (COPD). This is what reveals a study presented at the congress of the European Respiratory Society – which takes place in Amsterdam (the Netherlands) from September 26 to 30 – and published jointly in the Lancet Respiratory Medicine. 6 genetic variations influence lung health regardless of smoking.
At the origin of this study, a huge genetic database, UK Biobank. 50,000 samples were selected by the researchers. Among them, smokers and non-smokers with varied profiles: they were divided between weak, normal or very good respiratory capacity. The UK Biobank database has the advantage of measuring more than 800,000 genetic variants. Thanks to this high precision, the team of Professors Ian Hall and Martin Tobin was able to compare the impact of genes on lung health according to smoking status.
Better treat COPD
6 mutations act on the lungs independently of smoking, which would explain the development of COPD in non-smokers. For example, the number of duplications of a genome sequence on chromosome 17 influences lung health in both heavy smokers (35 pack-years) and non-smokers. Some variants are even thought to have a role in nicotine addiction.
These results have two consequences, explain the authors of the study. A better understanding of the mechanisms underlying the development of COPD will make it possible to prevent it but also to treat it better, by developing new therapeutic strategies.
“These results correspond to recent evidence for the different trajectories of lung function in the pathogenesis of COPD,” commented Prof. Guy Brusselle and Dr Ken Bracke, of the University Hospital of Ghent (Belgium) in a report. remark associated with the study. About half of patients experience an accelerated decline in lung function, while the other half will experience a normal decline, starting from a function already affected by the age of 20-40 years (…). Researchers have confirmed that the HHIP gene, which is involved in fetal lung development (…), is a COPD sensitivity gene. ”
These two practitioners are awaiting further studies of this type in order to further deepen our knowledge of the genetic markers of COPD.
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