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以肝脏巨噬细胞为靶点治疗非酒精性脂肪性肝病

Targeting hepatic macrophages for non-alcoholic fatty liver disease therapy.

作者信息

Tian Yingxin, Ni Yiming, Zhang Ting, Cao Yemin, Zhou Mingmei, Zhao Cheng

机构信息

Shanghai Traditional Chinese Medicine Integrated Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

出版信息

Front Cell Dev Biol. 2024 Sep 5;12:1444198. doi: 10.3389/fcell.2024.1444198. eCollection 2024.

DOI:10.3389/fcell.2024.1444198
PMID:39300994
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11410645/
Abstract

Non-alcoholic fatty liver disease (NAFLD) and its more advanced form, non-alcoholic steatohepatitis (NASH), have become global health challenges with significant morbidity and mortality rates. NAFLD encompasses several liver diseases, ranging from simple steatosis to more severe inflammatory and fibrotic forms. Ultimately, this can lead to liver cirrhosis and hepatocellular carcinoma. The intricate role of hepatic macrophages, particularly Kupffer cells (KCs) and monocyte-derived macrophages (MoMFs), in the pathogenesis of NAFLD and NASH, has received increasing attention. Hepatic macrophages can interact with hepatocytes, hepatic stellate cells, and endothelial cells, playing a crucial role in maintaining homeostasis. Paradoxically, they also participate in the pathogenesis of some liver diseases. This review highlights the fundamental role of hepatic macrophages in the pathogenesis of NAFLD and NASH, emphasizing their plasticity and contribution to inflammation and fibrosis, and hopes to provide ideas for subsequent experimental research and clinical treatment.

摘要

非酒精性脂肪性肝病(NAFLD)及其更严重的形式,非酒精性脂肪性肝炎(NASH),已成为全球性的健康挑战,具有较高的发病率和死亡率。NAFLD涵盖多种肝脏疾病,从单纯性脂肪变性到更严重的炎症和纤维化形式。最终,这可能导致肝硬化和肝细胞癌。肝巨噬细胞,特别是枯否细胞(KCs)和单核细胞衍生的巨噬细胞(MoMFs),在NAFLD和NASH发病机制中的复杂作用日益受到关注。肝巨噬细胞可与肝细胞、肝星状细胞和内皮细胞相互作用,在维持体内平衡中起关键作用。矛盾的是,它们也参与某些肝脏疾病的发病机制。本综述强调肝巨噬细胞在NAFLD和NASH发病机制中的重要作用,强调其可塑性以及对炎症和纤维化的贡献,希望为后续的实验研究和临床治疗提供思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d764/11410645/10aaea2ee02e/fcell-12-1444198-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d764/11410645/6c7e71df1178/fcell-12-1444198-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d764/11410645/36f32672d27b/fcell-12-1444198-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d764/11410645/10aaea2ee02e/fcell-12-1444198-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d764/11410645/6c7e71df1178/fcell-12-1444198-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d764/11410645/36f32672d27b/fcell-12-1444198-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d764/11410645/10aaea2ee02e/fcell-12-1444198-g003.jpg

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Cell Metab. 2024 Aug 6;36(8):1745-1763.e6. doi: 10.1016/j.cmet.2024.05.008. Epub 2024 Jun 7.
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IL4 receptor targeting enables nab-paclitaxel to enhance reprogramming of M2-type macrophages into M1-like phenotype via ROS-HMGB1-TLR4 axis and inhibition of tumor growth and metastasis.靶向白细胞介素4受体可使纳米白蛋白结合型紫杉醇通过活性氧-高迁移率族蛋白B1- Toll样受体4轴增强M2型巨噬细胞重编程为M1样表型,并抑制肿瘤生长和转移。
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通过生物信息学和机器学习鉴定膜性肾病和非酒精性脂肪性肝病中的关键基因
Front Immunol. 2025 Jun 5;16:1564288. doi: 10.3389/fimmu.2025.1564288. eCollection 2025.
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Metabolic Dysfunction-Associated Steatotic Liver Disease: Pathogenetic Links to Cardiovascular Risk.代谢功能障碍相关脂肪性肝病:与心血管风险的发病机制联系
Biomolecules. 2025 Jan 22;15(2):163. doi: 10.3390/biom15020163.
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自然杀伤细胞和单核细胞衍生的巨噬细胞的外泌体在激活肝星状细胞中的多样潜能。
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