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巨噬细胞作为肝纤维化的双向调节因子和潜在治疗靶点。

Macrophages Serve as Bidirectional Regulators and Potential Therapeutic Targets for Liver Fibrosis.

机构信息

Clinical Medical Research Center, The Second Affiliated Hospital of Guangxi Medical University, Nanning, 530007, Guangxi, China.

Guangxi International Travel Healthcare Centre (Port Clinic of Nanning Customs District), Nanning, 530021, Guangxi, China.

出版信息

Cell Biochem Biophys. 2023 Dec;81(4):659-671. doi: 10.1007/s12013-023-01173-w. Epub 2023 Sep 11.

DOI:10.1007/s12013-023-01173-w
PMID:37695501
Abstract

Liver fibrosis is a dynamic pathological process in which the structure and function of the liver abnormally change due to long-term complex inflammatory reactions and chronic liver injury caused by multiple internal and external factors. Previous studies believed that the activation of hepatic stellate cells is a critical part of the occurrence and development of liver fibrosis. However, an increasing number of studies have indicated that the macrophage plays an important role as a central regulator in liver fibrosis, and it directly affects the development and recovery of liver fibrosis. Studies of macrophages and liver fibrosis in the recent 10 years will be reviewed in this paper. This review will not only clarify the molecular mechanism of liver fibrosis regulated by macrophages but also provide new strategies and methods for ameliorating and treating liver fibrosis.

摘要

肝纤维化是一种动态的病理过程,由于多种内外因素引起的长期复杂炎症反应和慢性肝损伤,肝脏的结构和功能异常改变。先前的研究认为,肝星状细胞的激活是肝纤维化发生和发展的关键部分。然而,越来越多的研究表明,巨噬细胞作为肝纤维化中央调控器发挥着重要作用,它直接影响肝纤维化的发展和恢复。本文对近 10 年来巨噬细胞与肝纤维化的研究进行综述。该综述不仅阐明了巨噬细胞调节肝纤维化的分子机制,而且为改善和治疗肝纤维化提供了新的策略和方法。

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[Mechanisms of the Anti-Fibrotic Effect of Ginsenoside Rh on Hepatic Fibrosis].[人参皂苷Rh对肝纤维化抗纤维化作用的机制]
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本文引用的文献

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RNF41 orchestrates macrophage-driven fibrosis resolution and hepatic regeneration.环指蛋白 41 调控巨噬细胞驱动的肝纤维化消退和肝再生。
Sci Transl Med. 2023 Jul 12;15(704):eabq6225. doi: 10.1126/scitranslmed.abq6225.
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Macrophage Polarization and Its Role in Liver Disease.巨噬细胞极化及其在肝脏疾病中的作用。
Front Immunol. 2021 Dec 14;12:803037. doi: 10.3389/fimmu.2021.803037. eCollection 2021.
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Selective suppression of M1 macrophages is involved in zinc inhibition of liver fibrosis in mice.锌通过抑制 M1 型巨噬细胞而抑制肝纤维化。
PFKFB3 介导的糖酵解在肝纤维化作用和机制研究进展(综述)。
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Omega-3 Lipid Mediators: Modulation of the M1/M2 Macrophage Phenotype and Its Protective Role in Chronic Liver Diseases.ω-3 脂质介质:调节 M1/M2 巨噬细胞表型及其在慢性肝病中的保护作用。
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Functional interaction between macrophages and hepatocytes dictate the outcome of liver fibrosis.巨噬细胞和肝细胞之间的功能相互作用决定了肝纤维化的结局。
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Nat Rev Gastroenterol Hepatol. 2021 Mar;18(3):151-166. doi: 10.1038/s41575-020-00372-7. Epub 2020 Oct 30.
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