The role of the extracellular matrix and specific growth factors in the regulation of inflammation and remodelling in asthma

被引:43
作者
Burgess, Janette K. [1 ,2 ]
机构
[1] Univ Sydney, Discipline Pharmacol, Woolcock Inst Med Res, Sydney, NSW 2006, Australia
[2] Cooperat Res Ctr Asthma & Airways, Sydney, NSW 2006, Australia
基金
英国医学研究理事会;
关键词
Asthma; Airway remodelling; Extracellular matrix; Growth factors; Fibronectin; Transforming growth factor beta; AIRWAY-SMOOTH-MUSCLE; COLONY-STIMULATING FACTOR; HUMAN-LUNG FIBROBLASTS; BRONCHOALVEOLAR LAVAGE FLUID; BRONCHIAL EPITHELIAL-CELLS; GM-CSF PRODUCTION; FACTOR-BETA; BASEMENT-MEMBRANE COLLAGEN; HEPARAN SULFATE COMPLEXES; BLOOD MONONUCLEAR-CELLS;
D O I
10.1016/j.pharmthera.2008.12.002
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Asthma is a disease characterised by persistent inflammation and structural changes in the airways, referred to as airway remodelling. The mechanisms underlying these processes may be interdependent or they may be separate processes that are driven by common factors. The levels of a variety of growth factors (including transforming growth factor 1, granulocyte macrophage colony stimulating factor, and vascular endothelial growth factor) are known to be changed in the asthmatic airway. These and other growth factors can contribute to the development and persistence of inflammation and remodelling. One of the Prominent features of the structural changes of the airways is the increased deposition and alterations in the composition of the extracellular matrix proteins. These proteins include fibronectin, many different collagen types and hyaluronan. There is a dynamic relationship between the extracellular matrix proteins and the airway mesenchymal cells such that the changes in the extracellular Matrix proteins can also contribute to the persistence of inflammation and the airway remodelling. This review aims to summarise the role growth factors and extracellular matrix proteins play in the regulation of inflammation and airway remodelling in the asthmatic airway. (C) 2009 Published by Elsevier Inc.
引用
收藏
页码:19 / 29
页数:11
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