Black Judith L, Burgess Janette K, Johnson Peter R A
Department of Pharmacology, Woolcock Institute of Medical Research, University of Sydney, Sydney, NSW 2006, Australia.
Respir Physiol Neurobiol. 2003 Sep 16;137(2-3):339-46. doi: 10.1016/s1569-9048(03)00157-5.
The airway smooth muscle cell has a variety of properties, which confer on it the ability to participate actively in the inflammatory process and the remodeling events, which accompany severe, persistent asthma. Among these properties is its relationship to the extracellular matrix (ECM) with which it interacts by releasing matrix proteins, matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs). Muscle cells derived from asthmatic subjects proliferate faster, release a different profile of matrix proteins, produce more connective tissue growth factor (CTGF) in response to TGFbeta stimulation and these changes may impact on airway smooth muscle contraction and proliferation. Integrins on the surface of the airway smooth muscle transduce signals between the muscle cell and the ECM, but whether the expression and/or function of these is altered in asthma is not known. It is unlikely that current therapy is effective in preventing or reversing remodeling, and therefore, understanding the pathophysiological events, which underlie its mechanism is critical.
气道平滑肌细胞具有多种特性，使其能够积极参与炎症过程以及与严重持续性哮喘相关的重塑事件。这些特性包括它与细胞外基质（ECM）的关系，气道平滑肌细胞通过释放基质蛋白、基质金属蛋白酶（MMPs）及其组织抑制剂（TIMPs）与细胞外基质相互作用。来自哮喘患者的肌肉细胞增殖更快，释放不同类型的基质蛋白，在转化生长因子β（TGFβ）刺激下产生更多的结缔组织生长因子（CTGF），这些变化可能影响气道平滑肌的收缩和增殖。气道平滑肌表面的整合素在肌肉细胞和细胞外基质之间传导信号，但这些整合素的表达和/或功能在哮喘中是否改变尚不清楚。目前的治疗方法不太可能有效预防或逆转重塑，因此，了解其机制背后的病理生理事件至关重要。
