Function of cAMP scaffolds in obstructive lung disease: Focus on epithelial-to-mesenchymal transition and oxidative stress

被引:18
作者
Zuo, Haoxiao [1 ,2 ]
Cattani-Cavalieri, Isabella [2 ,3 ]
Valenca, Samuel Santos [3 ]
Musheshe, Nshunge [1 ]
Schmidt, Martina [1 ,2 ]
机构
[1] Univ Groningen, Dept Mol Pharmacol, Groningen, Netherlands
[2] Univ Groningen, Univ Med Ctr Groningen, GRIAC, Antonius Deusinglaan 1, NL-9713 AV Groningen, Netherlands
[3] Univ Fed Rio de Janeiro, Inst Biomed Sci, Rio De Janeiro, Brazil
关键词
KINASE ANCHORING PROTEINS; IDIOPATHIC PULMONARY-FIBROSIS; TGF-BETA ACTIVATION; ROFLUMILAST N-OXIDE; PHARMACOLOGY; 2017/18; CONCISE GUIDE; CIGARETTE-SMOKE; MOLECULAR-MECHANISMS; E-CADHERIN; RECEPTOR;
D O I
10.1111/bph.14605
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Over the past decades, research has defined cAMP as one of the central cellular nodes in sensing and integrating multiple pathways and as a pivotal role player in lung pathophysiology. Obstructive lung disorders, such as chronic obstructive pulmonary disease (COPD), are characterized by a persistent and progressive airflow limitation and by oxidative stress from endogenous and exogenous insults. The extent of airflow obstruction depends on the relative deposition of different constituents of the extracellular matrix, a process related to epithelial-to-mesenchymal transition, and which subsequently results in airway fibrosis. Oxidative stress from endogenous and also from exogenous sources causes a profound worsening of COPD. Here we describe how cAMP scaffolds and their different signalosomes in different subcellular compartments may contribute to COPD. Future research will require translational studies to alleviate disease symptoms by pharmacologically targeting the cAMP scaffolds. Linked Articles This article is part of a themed section on Adrenoceptors-New Roles for Old Players. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.14/issuetoc
引用
收藏
页码:2402 / 2415
页数:14
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