Therefore, studies on protein expression can enable better understanding of the pathological mechanism of bronchial asthma. Throughout the course of bronchial asthma, changes in the levels of transcription factors, inflammatory mediators, chemokines, cytokines, and cell apoptosis and proliferation-related proteins also take place ( 7). These changes can result in immune system imbalance, eventually leading to airway hyperresponsiveness ( 6). The main pathophysiological characteristics of asthma are inflammation and airway remodeling, which include goblet cell hyperplasia, subepithelial fibrosis, collagen deposition, mucosal gland hyperplasia, smooth muscle hypertrophy, and changes in the extracellular matrix. In addition, mutations in the ORM1 gene have been revealed in studies on single nucleotide polymorphisms (SNPs) to also be closely related to the onset of asthma ( 4, 5). In terms of genetic factors, a genome-wide association (GWA) study identified more than 100 genes as being significantly associated with the onset of bronchial asthma. Environmental substances that may cause asthma include indoor allergens (e.g., dust mites, pets, and cockroaches), outdoor allergens (e.g., pollen and dust), sources of infection (e.g., bacteria, fungi, and parasites), occupational pollutants, or food additives ( 3). In 2016, an estimated 300 million people worldwide had bronchial asthma by 2025, this number is expected to reach 400 million ( 1, 2).Īlthough the etiology of bronchial asthma remains unknown, its pathogenesis is well believed to be affected by both genetic and environmental factors. Epidemiological studies have revealed that there has been a worldwide increase in the prevalence of bronchial asthma over the past four decades. Bronchial asthma is a common chronic inflammatory disease of the airways characterized by reversible bronchospasm, which is caused by bronchial hyperreactivity.
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