Chen Li, Brigstock David R
The Research Institute at Nationwide Children's Hospital, Research Building 2, 700 Children's Drive, Columbus, OH, 43205, USA.
Molecular, Cellular, and Developmental Biology Program, The Ohio State University, Columbus, OH, 43212, USA.
Methods Mol Biol. 2017;1489:445-463. doi: 10.1007/978-1-4939-6430-7_37.
Hepatic fibrosis is a complex pathology arising from chronic injury. Pathological features are dominated by the excessive production of extracellular matrix proteins, particularly collagens which are deposited as insoluble scar material that can compromise tissue function. Fibrosis in the liver can often be assessed by staining for collagen in tissue sections and this is an approach that is widely used for grading of fibrosis in human biopsies. However, the recognition of the molecular components that drive fibrosis, including CCN proteins, and the involvement of hepatic stellate cells (HSC) as the principal collagen-producing cells in fibrosing liver, has resulted in a wide variety of molecular and cellular approaches to study the pathogenesis of fibrosis both in vivo and in vitro.
肝纤维化是一种由慢性损伤引起的复杂病理状态。其病理特征主要表现为细胞外基质蛋白过度产生,尤其是胶原蛋白,这些胶原蛋白以不溶性瘢痕物质的形式沉积,会损害组织功能。肝脏纤维化通常可通过对组织切片中的胶原蛋白进行染色来评估,这种方法广泛用于人类活检中纤维化的分级。然而,对驱动纤维化的分子成分(包括CCN蛋白)的认识,以及肝星状细胞(HSC)作为纤维化肝脏中主要胶原蛋白产生细胞的参与,导致了多种分子和细胞方法来研究体内和体外纤维化的发病机制。