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Novel perspectives on the origins of the hepatic myofibroblasts

机译：肝成肌纤维细胞起源的新颖观点

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Abstract: Liver fibrosis results from chronic liver injury that causes hepatocellular damage. Damaged hepatocytes apoptose, and release factors that facilitate recruitment of leukocytes to the site of injury, which in turn mediate recruitment and activation of liver- resident (Kupffer cells) and bone marrow (BM)-derived macrophages. Activated macrophages secrete TGF-?1, the major profibrogenic cytokine, which activates hepatic myofibroblasts, which are not present in the liver under physiological conditions. Several sources of myofibroblasts have been identified, but it is believed that liver-resident hepatic stellate cells (HSCs) and portal fibroblasts (PFs) are the major source of hepatic myofibroblasts in fibrotic liver. Fibrocytes, designated as BM-derived collagen Type I producing cells, were also implicated in liver fibrosis; hence, their contribution to liver fibrosis remains controversial. Upon removal of the etiological agent, myofibroblasts either undergo apoptosis or inactivate into a quiescent-like state, followed by resorbtion of the fibrous scar. However, prolonged/repeated liver injury triggers irreversible cross-linking of collagen fibers that prevents fibrous scar from collagenase-mediated degradation. This review will discuss several types of fibrogenic cells contributing to the myofibroblast population, and the signaling pathways regulating their activation and collagen deposition.
机译：摘要：肝纤维化是由慢性肝损伤导致的肝细胞损伤所致。受损的肝细胞凋亡，并释放促进白细胞募集到损伤部位的释放因子，继而介导肝驻留（库普弗细胞）和骨髓（BM）衍生的巨噬细胞的募集和激活。活化的巨噬细胞分泌TGF-β1，这是主要的纤维原性细胞因子，可活化肝脏的成纤维细胞，在生理条件下肝脏中不存在。已经鉴定出肌成纤维细胞的几种来源，但是据信肝脏驻留的肝星状细胞（HSC）和门静脉成纤维细胞（PF）是纤维化肝中肝成纤维细胞的主要来源。称为BM衍生I型胶原产生细胞的纤维细胞也与肝纤维化有关。因此，它们对肝纤维化的贡献仍存在争议。除去病原体后，成肌纤维细胞要么发生凋亡，要么失活成静止状态，然后再吸收纤维疤痕。但是，长时间/反复的肝损伤会触发胶原纤维的不可逆交联，从而防止胶原酶介导的降解引起纤维疤痕。这篇综述将讨论促成肌纤维母细胞群的几种类型的成纤维细胞，以及调节其活化和胶原沉积的信号传导途径。

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