Alterations in the composition of the extracellular matrix (ECM) and its abundance are important features of airway fibrosis, which is observed in lung disorders such as asthma, COPD and cystic fibrosis. The ECM was originally thought to only play a passive, structural role by providing a stable framework for the resident airway cells from which they are synthesized. However, there is now increasing evidence that the ECM impacts on the biological activity of smooth muscle cells, fibroblasts, and epithelial cells. Current anti-asthma therapy is only partially effective in preventing matrix deposition in chronic asthma, and does not reverse established fibrosis. Little is known about the signal transduction pathways that mediate ECM effects on airway smooth muscle cells. Importantly, in order for the ECM to influence myocyte phenotype and function, the cell must possess selective receptors (integrins) to induce intracellular signalling pathways. This mini-review explores current knowledge of the role of the ECM and its receptors (integrins) on airway smooth muscle phenotype and function and highlights their possible importance in airway disease. New signalling molecules that may be essential in mediating ECM-integrin interactions will also be discussed as they may prove to be novel targets for developing new therapies for asthma.
Keywords: Airway remodelling, apoptosis, asthma, βig-h3, caveolin, CD151, cell adhesion, collagen, COPD, extracellular matrix
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