PI3K/Akt信号通路在慢性阻塞性肺疾病中的研究进展

Research Progress on PI3K/Akt Signaling Pathway in Chronic Obstructive Pulmonary Disease

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一种常见的以持续气流受限为特征的慢性肺部疾病,其气流受限多呈进行性发展,与气道和肺组织经香烟烟雾等有害气体或有害颗粒刺激诱发的氧化应激和慢性炎症增强有关。目前,COPD的相关发病机制尚未完全明确。近年来,研究发现磷脂酰肌醇3激酶(phosphatidylinositol 3 kinase,PI3K)/蛋白激酶B(protein kinase B,Akt)信号通路参与调控COPD炎症和氧化应激反应以及类固醇的抵抗性,在COPD的发病机制和治疗中发挥关键作用。就PI3K/Akt的结构与转导过程和调控途径;与COPD炎症反应和氧化应激的关系;基于调控PI3K/Akt信号通路的COPD药物治疗进行综述,以期为临床干预COPD提供新的治疗靶点。

Chronic obstructive pulmonary disease(COPD)is a chronic lung disease characterized by airway inflammation and progressive obstruction of the lung airflow.In COPD,progression airflow obstruction occurs as a result of exposure to cigarette smoke,air pollution and fossil fuels,what are the risk factors mainly induce oxidative stress and inflammation,leading to abnormal of narrowing of the small airways.However,its pathogenesis is not completely known.Therefore,further research unraveling the underlying mechanisms is necessary.Extrinsic signaling pathways play crucial roles in COPD development and exacerbation.In particular,Phosphatidylinositol 3-kinase(PI3 K)/Akt signaling has recently been shown to be one of the most crucial pathways contributing to the pathophysiology such as inflammation and oxidative stress response as well as steroid resistance of COPD.This review aims to highlight the critical contribution of PI3 K/Akt signaling to the oxidative stress and inflammation of COPD.Moreover,we provide key question and suggestions utilizing the PI3 K/Akt signaling pathway for improving the therapeutic approaches for COPD.