New Mechanisms of Pulmonary Fibrosis
New Mechanisms of Pulmonary Fibrosis
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DOI：
10.1378/chest.09-0510
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发表时间：
2009-11-01
期刊：
影响因子：
9.6
通讯作者：
Mehrad, Borna
中科院分区：
文献类型：
--
作者：
Strieter, Robert M.;Mehrad, Borna
对肺纤维化发病机制的理解不断发展。最初的假设模型认为慢性炎症是肺纤维化的原因，而随后的假设认为上皮损伤和受损的伤口修复是纤维化的病因，而没有先前的炎症。在过去的十年中，几个概念已经导致这些假设的细化。其中包括：（1）肺泡-毛细血管屏障基底膜（BM）的完整性对保护损伤肺的结构的重要性;（2）相反，BM的再上皮化和再内皮化的失败导致病理性纤维化;（3）转化生长因子-β是肺的病理性纤维化所必需的，但不是充分的;（4）持久性抗原在普通型间质性肺炎发病机制中的作用;（5）上皮-间质转化和骨髓来源的祖细胞在肺纤维化发病机制中的作用。本文就特发性肺纤维化相关的肺纤维化发病机制进行综述。（CHEST 2009; 136：1364-1370）
The understanding of the pathogenesis of pulmonary fibrosis continues to evolve. The initial hypothetical model suggested chronic inflammation as the cause of pulmonary fibrosis, whereas a subsequent hypothesis posited epithelial injury and impaired wound repair as the etiology of fibrosis without preceding inflammation. Over the past decade, several concepts have led to refinement of these hypotheses. These include the following: (1) the importance of the integrity of the alveolar-capillary barrier basement membrane (BM) to conserving the architecture of the injured lung; (2) conversely, that the failure of reepithelialization and reendothelialization of this BM results in pathologic fibrosis; (3) transforming growth factor-beta is necessary but not sufficient to the pathologic fibrosis of the lungs; (4) the role of persistent antigens in the pathogenesis of usual interstitial pneumonia; and (5) the contribution of epithelial-to-mesenchymal transformation and bone marrow-derived progenitor cells in the pathogenesis of lung fibrosis. In this review, we will discuss these evolving conceptual mechanisms for the pathogenesis of pulmonary fibrosis relevant to idiopathic pulmonary fibrosis. (CHEST 2009; 136:1364-1370)