Lee Y C, Lane K B
Pulmonary Department, St. Thomas Hospital and Vanderbilt University, Nashville, Tennessee, USA.
Curr Opin Pulm Med. 2001 Jul;7(4):173-9. doi: 10.1097/00063198-200107000-00001.
Transforming growth factor (TGF)-beta is responsible for critical regulatory functions in many physiologic and pathologic processes. Emerging evidence suggests that these roles also apply to a multitude of pleural diseases. Both mesothelial cells and infiltrating cells in the pleural space can produce TGFbeta, and elevated TGFbeta concentrations have been found in pleural effusions and in pleural tissues during disease processes. Recent animal studies have suggested that TGFbeta can induce significant pleurodesis and probably plays a central role in the pathogenesis of pleural fibrosis. Paradoxically, TGFbeta may also stimulate increased pleural fluid formation, in part by inducing the production of vascular endothelial growth factor. TGFbeta also participates in the regulation of pleural inflammation and cell proliferation. Further research into the roles of TGFbeta in the pathogenesis of various pleural diseases is needed and may lead to the development of novel treatment strategies.
转化生长因子（TGF）-β在许多生理和病理过程中发挥关键的调节功能。新出现的证据表明，这些作用也适用于多种胸膜疾病。胸膜间皮细胞和胸膜腔内浸润细胞均可产生TGF-β，在疾病过程中，胸腔积液和胸膜组织中TGF-β浓度升高。最近的动物研究表明，TGF-β可诱导显著的胸膜固定术，可能在胸膜纤维化发病机制中起核心作用。矛盾的是，TGF-β也可能刺激胸腔积液生成增加，部分原因是诱导血管内皮生长因子的产生。TGF-β还参与胸膜炎症和细胞增殖的调节。需要对TGF-β在各种胸膜疾病发病机制中的作用进行进一步研究，这可能会带来新的治疗策略的发展。
