肝纤维化发生发展及逆转过程中肝巨噬细胞亚群分类

肝纤维化是由持续性损伤修复反应引起的,导致肝组织内细胞外基质异常沉积,进一步引发肝脏结构和肝功能异常改变的一种病理过程.已有大量研究表明,肝纤维化在去除损伤因素后是可以逆转的.肝星状细胞作为主要的效应细胞,合成和分泌各种胶原和细胞外基质,一直被认为是肝纤维化发生发展的中心环节.最近的研究发现,巨噬细胞作为主要的调节细胞,能同时调节肝星状细胞的功能和基质胶原的降解,促进肝纤维化的形成.而在肝纤维化逆转过程中,促使活化的肝星状细胞凋亡和纤维胶原的降解,促进肝纤维化的逆转.目前已有研究表明,巨噬细胞亚群在肝纤维化发生发展及逆转中具有双向调控作用,但是对于动物模型体内还没有系统的研究巨噬细胞亚群的分类.本文对巨噬细胞亚群的分类研究做一个全面的综述,对肝脏巨噬细胞在肝纤维化中分子机制的进一步研究具有一定的参考价值和借鉴意义.

Macrophage Subsets in the Development and Reversal of Liver Fibrosis

Liver fibrosis was caused by persistent injury-repair reactions, resulting in abnormal deposition of extracellular matrix in liver tissue, and further a pathological process caused by the abnormal changes of the liver structure and function. Hepatic stellate cells as a major effecter cells, synthesizing and secreting of collagen and extracellular matrix, have been considered to be the central link of the liver fibrosis development. However, researchers found that macrophages as the main regulating cells can regulate the function of hepatic stellate cells and degradation of matrix collagen. Macrophages can activate resting hepatic stellate cells in the process of liver fibrosis, promote the development of hepatic fibrosis, and promote a reversal of liver fibrosis by promoting apoptosis of activated hepatic stellate cells and degradation of fiber collagen. Studies now suggest that the pathogenesis of fibrosis is tightly regulated by distinct macrophage populations that exert unique functional activities throughout the initiation, maintenance, and resolution phases of fibrosis. But there is no systematic classification of macrophage subsets in vivo animal models. This article has a comprehensive review of the classification of macrophage subsets to have a certain reference value and significance for further study of the molecular mechanisms of liver macrophages in liver fibrosis.