PI3K/Akt信号通路在哮喘气道重塑中的研究进展

Research Progress of PI3K/Akt Signaling Pathway in the Reconstruction of Asthma Airway

哮喘是一种气道慢性炎症性疾病,长期的慢性炎症刺激可以导致气道结构改变,形成气道重塑。气道重塑可以导致气道痉挛的可逆性减弱或丧失,表现为对支气管扩张剂不敏感或持续性通气障碍,脱离变应原后气道仍呈高反应性,肺功能指标持续性降低,甚至对糖皮质激素不敏感,在气道重塑的基础上再继发感染可导致病情的迅速恶化,因此在治疗慢性炎症的同时需要预防气道重塑。许多临床试验研究提示阻断磷脂酰肌醇-3-激酶/蛋白激酶B信号转导通路可以通过多种机制抑制小鼠气道重塑。了解这些机制有利于进一步研究哮喘的临床治疗。

Asthma is a chronic airway inflammatory disease,and long chronic inflammatory stimulation can lead to the change of airway structure and form airway remodeling. Airway remodeling can lead to the weakening or loss of reversibility of airway spasm,manifested as insensitive to bronchodilator or continuous ventilation disorder,continuous high reactivity after allergen removal,continuing decrease of pulmonary function index,even insensitive to glucocorticoids. Secondary infection on the basis of the airway remodeling can result in rapid deterioration,so prevention of airway remodeling in the treatment of chronic inflammation is needed. Many clinical trials suggest that blocking the phosphatidylinositol-3-kinase/protein kinase B signaling pathway can inhibit airway remodeling in mice through various mechanisms. Understanding these mechanisms will help further study of the clinical treatment of asthma.