摘要
人们对特发性肺纤维化发病机制的认识在不断深入,早期理论认为慢性炎症是肺纤维化的基本病因,而随后的一系列理论则认为上皮细胞的损伤及其异常修复才是肺纤维化的病因,且与炎症无关。近年来,肺纤维化发病机制可以概括为以下几方面:(1)肺泡毛细血管屏障基底膜完整性的破坏作为肺纤维化形成的"不可逆点",导致肺组织的纤维化。(2)在基底膜完整性遭到破坏的情况下,上皮细胞和内皮细胞的再生失败会导致肺组织结构的破坏和病理性纤维化。(3)转化生长因子-β是纤维化的必要因素,但不足以导致永久性的纤维化。(4)持续的损伤/抗原/刺激是纤维化发展的必要条件。(5)上皮细胞向间充质细胞转化和骨髓干细胞是纤维化调节中重要的细胞机制。
The understanding of the pathogenesis of idiopathic pulmonary fibrosis continues to be deeper. The initial theory suggested that chronic inflammation is the basic cause of pulmonary fibrosis, whereas a series of subsequent theories demeonstrated that epithelial injury and abnormal repair is the etiology of fibrosis, and it is unrelated to inflammation. These theories include the following： （1） the loss of alveolar-capillary barrier basement membrane （BM） integrity represents the＂point of no return＂that results in the pathologic fibrosis. （2） The failure of reepithelialization and reendothelialization in the context of the loss of the BM integrity leads to destroy lung architecture and pathologic fibrosis. （3） Transforming growth factor-β（TGF-β） is necessary but not entirely sufficient to promote permanent fibrosis. （4） A persistent injury/antigen /irritant is necessary for the propagation of fibrosis. （5） Epithelial to mesenchymal transition （EMT） and a bone marrow derived progenitor cell are critical cellular mechanisms in the regulation of fibrosis.
出处
《武警后勤学院学报（医学版）》
CAS
2013年第1期69-73,共5页
Journal of Logistics University of PAP（Medical Sciences）
关键词
特发性肺纤维化
慢性炎症
发病机制
Idiopathic pulmonary fibrosis
Chronic inflammation
Pathogenesis
