Abstract

Background and ObjectiveBronchial asthma, a common respiratory disease in children and young adults, is characterized by hyperresponsiveness and reversible narrowing of the airways which manifest clinically as shortness of breath, cough, and/or wheezing. Although its pathogenic mechanism remains unknown, it’s known that asthma patients have substantial interindividual variability in drug responsiveness, among which genetic factors play key roles. For improving the understanding of the biological mechanism of asthma and useful recognition of diagnostic and therapeutic targets, and the main purpose of this article is to optimize drug selection by analyzing genes associated with different drug responsiveness in asthmatic patients through the use of genomic techniques.Methodsβ2-agonists, inhaled corticosteroids (ICS), and leukotriene modulators are the most commonly used to treat asthma, and major genetic variations associated with differential response to these three drugs were identified via candidate gene association analysis, genome-wide association study (GWAS), and RNA sequencing.Key Content and FindingsGenomics focuses on the effects of genetic variations in a group of genes. Most current studies have focused on the effect of single gene polymorphisms on drug efficacy, but the pharmacogenomics of asthma is inherently complex, with each factor having a small effect on drug responsiveness, and no single locus has yet been able to predict the variability in drug responsiveness.ConclusionsAccording to epidemiological researches, a worldwide increase in the prevalence of bronchial asthma over the past four decades was shown. Genomic approaches can be used to screen for genetic variants associated with drug response. Stratifying patients prior to treatment helps to optimize drug selection, maximize the effectiveness of individual treatment, and improve clinical outcomes.

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