Targeting PI3K/AKT signaling for treatment of idiopathic pulmonary fibrosis

查看全文 作　　者：Jincheng [1]Wang;Kaili [1,2]Hu;Xuanyan [1]Cai;Bo [2]Yang;Qiaojun [1,2]He;Jiajia [1]Wang;Qinjie [1,2]Weng

机构地区：[1]Center for Drug Safety Evaluation and Research,College of Pharmaceutical Sciences,Zhejiang University,Hangzhou 310058;[2]Hangzhou Institute of Innovative Medicine,College of Pharmaceutical Sciences,Zhejiang University,Hangzhou 310058

出　　处：《Acta Pharmaceutica Sinica B》索引2022年第12卷第1期,共15页

基　　金：supported by the National Natural Science Foundation of China(No.82003873);the Postdoctoral Science Foundation of China(No.2020M681899);the Zhejiang Provincial Natural Science Foundation of China(No.LR21H310001)。 摘　　要：Idiopathic pulmonary fibrosis(IPF) is a chronic progressive fibrotic interstitial pneumonia with unknown causes. The incidence rate increases year by year and the prognosis is poor without cure.Recently, phosphatidylinositol 3-kinase(PI3 K)/protein kinase B(PKB/AKT) signaling pathway can be considered as a master regulator for IPF. The contribution of the PI3 K/AKT in fibrotic processes is increasingly prominent, with PI3 K/AKT inhibitors currently under clinical evaluation in IPF. Therefore,PI3 K/AKT represents a critical signaling node during fibrogenesis with potential implications for the development of novel anti-fibrotic strategies. This review epitomizes the progress that is being made in understanding the complex interpretation of the cause of IPF, and demonstrates that PI3 K/AKT can directly participate to the greatest extent in the formation of IPF or cooperate with other pathways to promote the development of fibrosis. We further summarize promising PI3 K/AKT inhibitors with IPF treatment benefits, including inhibitors in clinical trials and pre-clinical studies and natural products, and discuss how these inhibitors mitigate fibrotic progression to explore possible potential agents, which will help to develop effective treatment strategies for IPF in the near future. 关键词：Idiopathic pulmonary fibrosis PI3K/AKT signaling PATHOGENESIS Coagulation cascade Immune activation Fibroblast accumulation Therapeutic target Drug therapy

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Targeting PI3K/AKT signaling for treatment of idiopathic pulmonary fibrosis

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