Hepatic stellate cell activation and pro-fibrogenic signals.

Hepatic stellate cell activation and pro-fibrogenic signals.
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DOI:
10.1016/j.jhep.2017.06.001
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发表时间:
2017-11
影响因子:
25.7
通讯作者:
Gandhi CR
Gandhi CR
中科院分区:
医学1区
文献类型:
--
作者:
Gandhi CR

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肝纤维化是对包括代谢异常、病毒(丙型肝炎和B病毒[HCV/HBV])和其他感染、毒素和药物在内的病因学损伤的主要反应。慢性暴露于损伤剂可导致纤维化进展为不可逆的肝硬化。尽管现在已有针对HCV诱导的纤维化的有效疗法,但新的挑战是由于非酒精性和酒精性脂肪性肝炎引起的肝纤维化/肝硬化的惊人增加。明确肝纤维化/肝硬化的发生机制是非常重要的,无论病因如何,肝星状细胞(hepatic stellate cells,HSCs)都是肝纤维化/肝硬化的主要参与者。骨髓来源的纤维细胞、上皮-间充质转化和门静脉成纤维细胞(Pfb)是其他来源,但它们的贡献要低得多。Pfb在疾病的早期阶段很重要,但HSC主要负责疾病的进展,甚至是胆道纤维化。[1],[2]
Liver fibrosis is a primary response to injury of etiologies including metabolic abnormalities, viral (hepatitis C and B virus [HCV/HBV]) and other infections, toxins and drugs. Chronic exposure to the injury agent (s) can cause fibrosis to progress to irreversible cirrhosis. Although effective therapies for HCV-induced fibrosis are now available, the new challenge is the alarming increase in liver fibrosis/cirrhosis due to non-alcoholic and alcoholic steatohepatitis. A clear understanding of the mechanisms of hepatic fibrosis/cirrhosis is critical.Regardless of etiology, hepatic stellate cells (HSCs) are the major contributors to fibrosis/cirrhosis. Bone marrow-derived fibrocytes, epithelial-to-mesenchymal transition and portal fibroblasts (Pfb) are other sources, but their contribution is much lower. Pfb are important in the early stages of the disease, but HSCs are predominantly responsible for the progression of the disease, even for biliary fibrosis.[1],[2]
DOI: 10.4049/jimmunol.1400861
发表时间: 2014-10-15
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