The role of gene-ambient air pollution interactions in paediatric asthma

被引:8
|
作者
Kelchtermans, Jelte [1 ,2 ,3 ]
Hakonarson, Hakon [1 ,2 ,3 ]
机构
[1] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA
[2] Childrens Hosp Philadelphia, Ctr Appl Genom, Philadelphia, PA 19104 USA
[3] Childrens Hosp Philadelphia, Div Pulm Med, Philadelphia, PA 19104 USA
来源
EUROPEAN RESPIRATORY REVIEW | 2022年 / 31卷 / 166期
基金
美国国家卫生研究院;
关键词
S-TRANSFERASE P1; TUMOR-NECROSIS-FACTOR; CHILDHOOD ASTHMA; OXIDATIVE STRESS; ANTIOXIDANT SUPPLEMENTATION; OZONE EXPOSURE; LUNG-FUNCTION; RISK-FACTORS; CHILDREN; HEALTH;
D O I
10.1183/16000617.0094-2022
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Globally, asthma prevention and treatment remain a challenge. Ambient air pollution (AAP) is an environmental risk factor of special interest in asthma research. AAP is poorly defined and has been subdivided either by the origin of the air pollution or by the specific bioactive compounds. The link between AAP exposure and asthma exacerbations is well established and has been extensively reviewed. In this narrative review, we discuss the specific genetic variants that have been associated with increased AAP sensitivity and impact in paediatric asthma. We highlight the relative importance of variants associated with genes with a role in oxidant defences and the nuclear factor-kappa B pathway supporting a potential central role for these pathways in AAP sensitivity.
引用
收藏
页数:12
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