Progression of the PI3K/Akt signaling pathway in chronic obstructive pulmonary disease

被引:27
作者
Liu, Yanhui [1 ]
Kong, Haobo [2 ]
Cai, Heping [1 ]
Chen, Guanru [1 ]
Chen, Huiying [1 ]
Ruan, Wenyi [1 ]
机构
[1] Anhui Prov Childrens Hosp, Dept Clin Pharm, Hefei, Anhui, Peoples R China
[2] Anhui Chest Hosp, Dept Resp Intens Care Unit, Hefei, Anhui, Peoples R China
关键词
chronic obstructive pulmonary disease; PI3K/Akt signalling pathway; inhibitor; inflammation; oxidative stress; REVERSES CORTICOSTEROID INSENSITIVITY; OXIDATIVE STRESS; PHOSPHOINOSITIDE; 3-KINASES; TUMOR-SUPPRESSOR; INFLAMMATION; CANCER; AKT; ERYTHROMYCIN; INHIBITION; KINASE;
D O I
10.3389/fphar.2023.1238782
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Chronic Obstructive Pulmonary Disease (COPD) is a chronic respiratory disease characterized by a slow progression and caused by the inhalation of harmful particulate matter. Cigarette smoke and air pollutants are the primary contributing factors. Currently, the pathogenesis of COPD remains incompletely understood. The PI3K/Akt signaling pathway has recently emerged as a critical regulator of inflammation and oxidative stress response in COPD, playing a pivotal role in the disease's progression and treatment. This paper reviews the association between the PI3K/Akt pathway and COPD, examines effective PI3K/Akt inhibitors and novel anti-COPD agents, aiming to identify new therapeutic targets for clinical intervention in this disease.
引用
收藏
页数:9
相关论文
共 97 条
[1]   The critical role of Akt in cardiovascular function [J].
Abeyrathna, Prasanna ;
Su, Yunchao .
VASCULAR PHARMACOLOGY, 2015, 74 :38-48
[2]   Oxidative stress dependent microRNA-34a activation via PI3Kα reduces the expression of sirtuin-1 and sirtuin-6 in epithelial cells [J].
Baker, J. R. ;
Vuppusetty, C. ;
Colley, T. ;
Papaioannou, Andriana I. ;
Fenwick, P. ;
Donnelly, Louise ;
Ito, K. ;
Barnes, P. J. .
SCIENTIFIC REPORTS, 2016, 6
[3]   Oxidative Stress in Chronic Obstructive Pulmonary Disease [J].
Barnes, Peter J. .
ANTIOXIDANTS, 2022, 11 (05)
[4]   Cellular Senescence as a Mechanism and Target in Chronic Lung Diseases [J].
Barnes, Peter J. ;
Baker, Jonathan ;
Donnelly, Louise E. .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2019, 200 (05) :556-564
[5]   Inflammatory mechanisms in patients with chronic obstructive pulmonary disease [J].
Barnes, Peter J. .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2016, 138 (01) :16-27
[6]   Differential Effects of p38, MAPK, PI3K or Rho Kinase Inhibitors on Bacterial Phagocytosis and Efferocytosis by Macrophages in COPD [J].
Bewley, Martin A. ;
Belchamber, Kylie B. R. ;
Chana, Kirandeep K. ;
Budd, Richard C. ;
Donaldson, Gavin ;
Wedzicha, Jadwiga A. ;
Brightling, Christopher E. ;
Kilty, Lain ;
Donnelly, Louise E. ;
Barnes, Peter J. ;
Singh, Dave ;
Whyte, Moira K. B. ;
Dockrell, David H. .
PLOS ONE, 2016, 11 (09)
[7]   Does the Interdependence between Oxidative Stress and Inflammation Explain the Antioxidant Paradox? [J].
Biswas, Subrata Kumar .
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2016, 2016
[8]   Reactive Oxygen Species in Chronic Obstructive Pulmonary Disease [J].
Boukhenouna, Samia ;
Wilson, Mark A. ;
Bahmed, Karim ;
Kosmider, Beata .
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2018, 2018
[9]   Airway inflammation in COPD: progress to precision medicine [J].
Brightling, Christopher ;
Greening, Neil .
EUROPEAN RESPIRATORY JOURNAL, 2019, 54 (02)
[10]   Risk factors for and origins of COPD [J].
Byrne, Anthony L. ;
Marais, Ben J. ;
Mitnick, Carole D. ;
Lecca, Leonid ;
Marks, Guy B. .
LANCET, 2015, 385 (9979) :1723-1724