CAJ | 학술논문

正常情况下气道黏膜下腺体在MUC5B调控下分泌少量黏液,具有吸附吸入的微粒及病原菌等屏障作用;病理状态下存在黏液细胞增生、化生,黏液过度分泌导致气道狭窄.气道黏液高分泌的机制复杂,且针对高分泌目前缺乏有效治疗手段.新近研究显示,气道黏蛋白基因上调及其下游信号的激活是上述病理改变的基础.调控黏蛋白基因抑或成为未来治疗气道黏液高分泌的方向.
정상정황하기도점막하선체재MUC5B조공하분비소량점액,구유흡부흡입적미립급병원균등병장작용;병리상태하존재점액세포증생、화생,점액과도분비도치기도협착.기도점액고분비적궤제복잡,차침대고분비목전결핍유효치료수단.신근연구현시,기도점단백기인상조급기하유신호적격활시상술병리개변적기출.조공점단백기인억혹성위미래치료기도점액고분비적방향.
Normal airway mucus is secreted from glands under airway epithelium and modulated by MUC5B. Mucus lines airway surface provides an important function by trapping and removing pathogens and particulates. However, in some pathologic conditions, such as asthma, there are mucous cells hyperplasia and metaplasia. Overproduction and secretion of mucus lead to airway narrow. The mechanism of mucus hypersecretion is complicated,and it is deficiency in overcoming mucus hypersecreion so far. It is showed that up-regulation of mucin genes and down stream signals activation are the major mechanisms of mucus overproduction and secretion, and mucin gene modulation might be the direction in treating pathologic airway mucus hypersecretion.