Kisseleva Tatiana, Brenner David A
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Proc Am Thorac Soc. 2008 Apr 15;5(3):338-42. doi: 10.1513/pats.200711-168DR.
Fibrosis of parenchymal organs is caused by prolonged injury, deregulation of the normal processes of wound healing, and extensive deposition of extracellular matrix (ECM) proteins. The current review will focus on common features of fibrogenesis in parenchymal organs, and will briefly discuss common features and differences in the pathophysiology of fibrosis. Comparison of hepatic, renal, and pulmonary fibrosis has identified several common mechanisms. Common themes include a critical role for the cytokine transforming growth factor beta and the generation of reactive oxygen species. Activated myofibroblasts are the common cell type that produce the excessive fibrous scar and may originate from endogenous cells such as hepatic stellate cells or fibroblasts, from the bone marrow such as fibrocytes, or from the transition of epithelial cells to mesenchymal cells. These concepts open new prospects for multidisciplinary research and the development of new therapies for fibrosis.
实质器官纤维化是由长期损伤、正常伤口愈合过程失调以及细胞外基质（ECM）蛋白的大量沉积引起的。本综述将聚焦于实质器官纤维化形成的共同特征，并简要讨论纤维化病理生理学中的共同特征和差异。肝纤维化、肾纤维化和肺纤维化的比较已确定了几种共同机制。共同主题包括细胞因子转化生长因子β的关键作用和活性氧的产生。活化的肌成纤维细胞是产生过多纤维瘢痕的常见细胞类型，其可能起源于内源性细胞，如肝星状细胞或成纤维细胞；起源于骨髓，如纤维细胞；或起源于上皮细胞向间充质细胞的转变。这些概念为纤维化的多学科研究和新疗法的开发开辟了新前景。
