Wells Rebecca G, Schwabe Robert F
Departments of Medicine (GI) and Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Semin Liver Dis. 2015 May;35(2):97-106. doi: 10.1055/s-0035-1550061. Epub 2015 May 14.
Liver fibrosis contributes to many of the devastating complications of viral, toxic, fatty, and cholestatic liver disease. Understanding the cell populations that promote liver fibrosis and the molecular pathways through which they operate is essential for the development of antifibrotic therapies. The authors review the origins and functions of hepatic myofibroblasts, focusing on hepatic stellate cells, the main contributors to organ fibrosis, and portal fibroblasts, an insufficiently characterized population that may have a specialized function in promoting periductular fibrosis, but a limited role in overall organ fibrosis. They discuss the hypothesis that each fibrogenic cell population in the liver exerts specific functions, and whether cell type-specific antifibrotic strategies are required or whether one therapeutic strategy fits all.
肝纤维化是病毒性、中毒性、脂肪性和胆汁淤积性肝病许多严重并发症的成因。了解促进肝纤维化的细胞群及其作用的分子途径对于抗纤维化治疗的开发至关重要。作者综述了肝肌成纤维细胞的起源和功能，重点关注肝星状细胞（器官纤维化的主要促成细胞）和门周成纤维细胞（这一特征尚不充分的细胞群可能在促进小叶间胆管周围纤维化方面具有特殊功能，但在整个器官纤维化中作用有限）。他们讨论了肝脏中每种促纤维化细胞群发挥特定功能的假说，以及是否需要针对特定细胞类型的抗纤维化策略，还是一种治疗策略适用于所有情况。
