The extracellular matrix and mechanotransduction in pulmonary fibrosis
The extracellular matrix and mechanotransduction in pulmonary fibrosis
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DOI：
10.1016/j.biocel.2020.105802
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发表时间：
2020-09-01
影响因子：
4
通讯作者：
Prele, Cecilia M.
中科院分区：
文献类型：
--
作者：
Deng, Zhenjun;Fear, Mark W.;Prele, Cecilia M.
肺纤维化的特征是肺中的过度瘢痕化，这导致肺功能受损，严重的呼吸问题，并且在某些疾病中导致死亡。它包括几种肺部疾病，其中特发性肺纤维化（IPF）是最常见和最严重的。肺纤维化被认为是通过异常伤口愈合而持续的，异常伤口愈合导致成纤维细胞积累、分化和活化，以及过量的细胞外基质（ECM）组分（特别是胶原蛋白）的沉积。最近的研究已经确定了在肺纤维化的发展过程中肺ECM的组成和结构的变化以及ECM和肺细胞之间的相互作用的重要性。有强有力的证据表明，增加的基质硬度诱导细胞功能的变化，包括增殖，迁移，分化和活化。了解ECM微环境的变化如何影响纤维化过程中的细胞行为，以及调节这些变化的机制，将为开发新的治疗方法提供见解。
Pulmonary fibrosis is characterised by excessive scarring in the lung which leads to compromised lung function, serious breathing problems and in some diseases, death. It includes several lung disorders with idiopathic pulmonary fibrosis (IPF) the most common and most severe. Pulmonary fibrosis is considered to be perpetuated by aberrant wound healing which leads to fibroblast accumulation, differentiation and activation, and deposition of excessive amounts of extracellular matrix (ECM) components, in particular, collagen. Recent studies have identified the importance of changes in the composition and structure of lung ECM during the development of pulmonary fibrosis and the interaction between ECM and lung cells. There is strong evidence that increased matrix stiffness induces changes in cell function including proliferation, migration, differentiation and activation. Understanding how changes in the ECM microenvironment influence cell behaviour during fibrogenesis, and the mechanisms regulating these changes, will provide insight for developing new treatments.