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肝脏炎症和纤维化。

Liver inflammation and fibrosis.

作者信息

Koyama Yukinori, Brenner David A

出版信息

J Clin Invest. 2017 Jan 3;127(1):55-64. doi: 10.1172/JCI88881.

DOI:10.1172/JCI88881
PMID:28045404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5199698/
Abstract

Chronic liver inflammation leads to fibrosis and cirrhosis, which is the 12th leading cause of death in the United States. Hepatocyte steatosis is a component of metabolic syndrome and insulin resistance. Hepatic steatosis may be benign or progress to hepatocyte injury and the initiation of inflammation, which activates immune cells. While Kupffer cells are the resident macrophage in the liver, inflammatory cells such as infiltrating macrophages, T lymphocytes, neutrophils, and DCs all contribute to liver inflammation. The inflammatory cells activate hepatic stellate cells, which are the major source of myofibroblasts in the liver. Here we review the initiation of inflammation in the liver, the liver inflammatory cells, and their crosstalk with myofibroblasts.

摘要

慢性肝脏炎症会导致肝纤维化和肝硬化,肝硬化是美国第12大死因。肝细胞脂肪变性是代谢综合征和胰岛素抵抗的一个组成部分。肝脂肪变性可能是良性的,也可能进展为肝细胞损伤并引发炎症,进而激活免疫细胞。虽然库普弗细胞是肝脏中的常驻巨噬细胞,但浸润性巨噬细胞、T淋巴细胞、中性粒细胞和树突状细胞等炎症细胞都会导致肝脏炎症。这些炎症细胞激活肝星状细胞,而肝星状细胞是肝脏中肌成纤维细胞的主要来源。在此,我们综述肝脏炎症的起始、肝脏炎症细胞及其与肌成纤维细胞的相互作用。

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