• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

巨噬细胞极化与肝缺血再灌注损伤

Macrophage Polarization and Liver Ischemia-Reperfusion Injury.

机构信息

Department of Liver Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.

出版信息

Int J Med Sci. 2021 Jan 1;18(5):1104-1113. doi: 10.7150/ijms.52691. eCollection 2021.

DOI:10.7150/ijms.52691
PMID:33526969
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7847630/
Abstract

Ischemia-reperfusion injury refers to organ damage caused by the previous insufficient supply of oxygen and nutrients and the involvement of metabolic by-products after blood flow is restored. Liver ischemia-reperfusion injury (IRI) has become a hot research in recent years, because it occurs in many clinical scenarios. After the introduction of liver transplantation and vascular control techniques in liver surgery, liver ischemia-reperfusion injury is considered to be an important factor affecting postoperative mortality and morbidity. As the largest immune organ in the human body, liver contain a lot of immune cells such as resident macrophages (Kupffer cells), dendritic cells, natural killer cells, and natural killer T cells which play a key role in ischemia-reperfusion injury. Among those, macrophage-mediated excessive inflammatory response is considered to be an important factor in liver ischemia-reperfusion injury. The prominent feature of liver injury is an increase in the number of macrophages in liver due to the infiltration of blood monocytes and differentiation into monocyte-derived macrophages. Liver macrophages can be divided into M1 macrophages which can promote inflammation progress and M2 macrophages that inhibit inflammation progress according to their different phenotypes and functions. Both of them can regulate liver aseptic inflammation, and play an important role in triggering, maintaining, and improving liver ischemia-reperfusion injury. This review summarizes studies of macrophage polarization on liver ischemia-reperfusion injury in recent years, to provide potential ideas for translation application in future clinical management.

摘要

缺血再灌注损伤是指先前氧和营养物质供应不足,血流恢复后代谢产物介入而导致的器官损伤。肝缺血再灌注损伤(IRI)近年来成为研究热点,因为它发生在许多临床情况下。在肝移植和血管控制技术引入肝外科后,肝缺血再灌注损伤被认为是影响术后死亡率和发病率的重要因素。作为人体最大的免疫器官,肝脏含有大量免疫细胞,如驻留巨噬细胞(库普弗细胞)、树突状细胞、自然杀伤细胞和自然杀伤 T 细胞,它们在缺血再灌注损伤中发挥关键作用。其中,巨噬细胞介导的过度炎症反应被认为是肝缺血再灌注损伤的重要因素。肝损伤的突出特征是由于血液单核细胞的浸润和分化为单核细胞衍生的巨噬细胞,导致肝脏巨噬细胞数量增加。肝脏巨噬细胞可根据其不同的表型和功能分为促进炎症进展的 M1 巨噬细胞和抑制炎症进展的 M2 巨噬细胞。它们都可以调节肝脏无菌性炎症,并在触发、维持和改善肝缺血再灌注损伤方面发挥重要作用。本综述总结了近年来关于巨噬细胞极化对肝缺血再灌注损伤的研究,为未来临床管理中的转化应用提供了潜在思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e0/7847630/bbe6331884dd/ijmsv18p1104g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e0/7847630/68fca6be2b76/ijmsv18p1104g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e0/7847630/bbe6331884dd/ijmsv18p1104g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e0/7847630/68fca6be2b76/ijmsv18p1104g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e0/7847630/bbe6331884dd/ijmsv18p1104g002.jpg

相似文献

1
Macrophage Polarization and Liver Ischemia-Reperfusion Injury.巨噬细胞极化与肝缺血再灌注损伤
Int J Med Sci. 2021 Jan 1;18(5):1104-1113. doi: 10.7150/ijms.52691. eCollection 2021.
2
Hyperglycemia-Triggered Sphingosine-1-Phosphate and Sphingosine-1-Phosphate Receptor 3 Signaling Worsens Liver Ischemia/Reperfusion Injury by Regulating M1/M2 Polarization.高血糖诱导的鞘氨醇-1-磷酸及其受体 3 信号通过调控 M1/M2 极化加重肝脏缺血再灌注损伤。
Liver Transpl. 2019 Jul;25(7):1074-1090. doi: 10.1002/lt.25470. Epub 2019 Jun 3.
3
Effect of Hepatic Macrophage Polarization and Apoptosis on Liver Ischemia and Reperfusion Injury During Liver Transplantation.肝巨噬细胞极化和凋亡对肝移植过程中肝脏缺血再灌注损伤的影响。
Front Immunol. 2020 Jun 26;11:1193. doi: 10.3389/fimmu.2020.01193. eCollection 2020.
4
Myeloid HO-1 modulates macrophage polarization and protects against ischemia-reperfusion injury.髓系 HO-1 调节巨噬细胞极化并防止缺血再灌注损伤。
JCI Insight. 2018 Oct 4;3(19):120596. doi: 10.1172/jci.insight.120596.
5
Myeloid Deletion of Cdc42 Protects Liver From Hepatic Ischemia-Reperfusion Injury via Inhibiting Macrophage-Mediated Inflammation in Mice.Cdc42 在髓系细胞中的缺失通过抑制巨噬细胞介导的炎症反应保护小鼠肝脏免受肝缺血再灌注损伤。
Cell Mol Gastroenterol Hepatol. 2024;17(6):965-981. doi: 10.1016/j.jcmgh.2024.01.023. Epub 2024 Feb 9.
6
Inflammasome-Mediated Inflammation in Liver Ischemia-Reperfusion Injury.炎症小体介导体缺血再灌注损伤中的炎症反应。
Cells. 2019 Sep 23;8(10):1131. doi: 10.3390/cells8101131.
7
Natural Killer Cells in Hepatic Ischemia-Reperfusion Injury.肝缺血再灌注损伤中的自然杀伤细胞
Front Immunol. 2022 Mar 28;13:870038. doi: 10.3389/fimmu.2022.870038. eCollection 2022.
8
Acidic Microenvironment Aggravates the Severity of Hepatic Ischemia/Reperfusion Injury by Modulating M1-Polarization Through Regulating PPAR-γ Signal.酸性微环境通过调节 PPAR-γ 信号调控 M1 极化加重肝缺血/再灌注损伤的严重程度。
Front Immunol. 2021 Jun 21;12:697362. doi: 10.3389/fimmu.2021.697362. eCollection 2021.
9
Prolonged Ischemia Triggers Necrotic Depletion of Tissue-Resident Macrophages To Facilitate Inflammatory Immune Activation in Liver Ischemia Reperfusion Injury.长时间缺血引发组织驻留巨噬细胞的坏死性消耗,以促进肝缺血再灌注损伤中的炎性免疫激活。
J Immunol. 2017 May 1;198(9):3588-3595. doi: 10.4049/jimmunol.1601428. Epub 2017 Mar 13.
10
Inhibiting ATP6V0D2 Aggravates Liver Ischemia-Reperfusion Injury by Promoting NLRP3 Activation via Impairing Autophagic Flux Independent of Notch1/Hes1.抑制 ATP6V0D2 通过损害自噬通量而非 Notch1/Hes1 促进 NLRP3 活化加重肝缺血再灌注损伤。
J Immunol Res. 2021 Mar 29;2021:6670495. doi: 10.1155/2021/6670495. eCollection 2021.

引用本文的文献

1
Mechanism of miR-107/HMOX1 axis in hepatic sinusoidal endothelial cells stimulated by ischemia-reperfusion injury.miR-107/HMOX1轴在缺血再灌注损伤刺激的肝窦内皮细胞中的作用机制
Hereditas. 2025 Jul 16;162(1):133. doi: 10.1186/s41065-025-00495-4.
2
Molecular Mechanisms of Ischemia/Reperfusion Injury and Graft Dysfunction in Liver Transplantation: Insights from Multi-Omics Studies in Rodent Animal Models.肝移植中缺血/再灌注损伤及移植物功能障碍的分子机制:来自啮齿动物模型多组学研究的见解
Int J Biol Sci. 2025 Feb 24;21(5):2135-2154. doi: 10.7150/ijbs.109449. eCollection 2025.
3
Lactylation: a promising therapeutic target in ischemia-reperfusion injury management.

本文引用的文献

1
Heme Oxygenase-1 in liver transplant ischemia-reperfusion injury: From bench-to-bedside.肝移植缺血再灌注损伤中的血红素加氧酶-1:从基础到临床。
Free Radic Biol Med. 2020 Sep;157:75-82. doi: 10.1016/j.freeradbiomed.2020.02.012. Epub 2020 Feb 19.
2
p300/CBP inhibitor A-485 alleviates acute liver injury by regulating macrophage activation and polarization.p300/CBP抑制剂A-485通过调节巨噬细胞活化和极化减轻急性肝损伤。
Theranostics. 2019 Oct 22;9(26):8344-8361. doi: 10.7150/thno.30707. eCollection 2019.
3
MSC-Derived Exosome Promotes M2 Polarization and Enhances Cutaneous Wound Healing.
乳酰化:缺血再灌注损伤管理中有前景的治疗靶点。
Cell Death Discov. 2025 Mar 13;11(1):100. doi: 10.1038/s41420-025-02381-4.
4
Macrophage expression of constitutively active alleviates hepatic injury in a mouse model of concanavalin A-induced autoimmune hepatitis.组成型活性巨噬细胞的表达减轻了刀豆蛋白A诱导的自身免疫性肝炎小鼠模型中的肝损伤。
Heliyon. 2025 Feb 13;11(4):e42691. doi: 10.1016/j.heliyon.2025.e42691. eCollection 2025 Feb 28.
5
Genome-wide KAS-Seq mapping of leukocytes in ischemia-reperfusion model reveals IL7R as a potential therapeutic target for ischemia-reperfusion injury.缺血再灌注模型中白细胞的全基因组KAS-Seq图谱揭示IL7R是缺血再灌注损伤的潜在治疗靶点。
Sci Rep. 2025 Feb 20;15(1):6165. doi: 10.1038/s41598-025-90457-7.
6
Understanding immunological insights of liver transplantation: a practice for attaining operational tolerance.理解肝移植的免疫学见解:实现手术耐受的实践。
Clin Exp Immunol. 2025 Jan 21;219(1). doi: 10.1093/cei/uxae125.
7
4-Octyl Itaconate Alleviates Myocardial Ischemia-Reperfusion Injury Through Promoting Angiogenesis via ERK Signaling Activation.衣康酸4-辛酯通过激活ERK信号通路促进血管生成减轻心肌缺血-再灌注损伤
Adv Sci (Weinh). 2025 Mar;12(10):e2411554. doi: 10.1002/advs.202411554. Epub 2025 Jan 21.
8
Blockade of the mitochondrial DNA release ameliorates hepatic ischemia-reperfusion injury through avoiding the activation of cGAS-Sting pathway.阻断线粒体 DNA 释放通过避免 cGAS-Sting 通路的激活减轻肝缺血再灌注损伤。
J Transl Med. 2024 Aug 28;22(1):796. doi: 10.1186/s12967-024-05588-8.
9
Current status and perspective on molecular targets and therapeutic intervention strategy in hepatic ischemia-reperfusion injury.肝缺血再灌注损伤中分子靶点及治疗干预策略的现状和展望。
Clin Mol Hepatol. 2024 Oct;30(4):585-619. doi: 10.3350/cmh.2024.0222. Epub 2024 Jul 1.
10
Novel anti-inflammatory peptide alleviates liver ischemia-reperfusion injury.新型抗炎肽减轻肝脏缺血再灌注损伤。
J Biomed Res. 2024 May 29;39(1):61-75. doi: 10.7555/JBR.38.20240020.
间充质干细胞衍生外泌体促进M2极化并增强皮肤伤口愈合。
Stem Cells Int. 2019 Sep 9;2019:7132708. doi: 10.1155/2019/7132708. eCollection 2019.
4
Gut microbiota-stimulated cathepsin K secretion mediates TLR4-dependent M2 macrophage polarization and promotes tumor metastasis in colorectal cancer.肠道微生物群刺激组织蛋白酶 K 的分泌,介导 TLR4 依赖性 M2 巨噬细胞极化,并促进结直肠癌的肿瘤转移。
Cell Death Differ. 2019 Nov;26(11):2447-2463. doi: 10.1038/s41418-019-0312-y. Epub 2019 Mar 8.
5
α-ketoglutarate attenuates ischemia-reperfusion injury of liver graft in rats.α-酮戊二酸减轻大鼠肝移植物缺血再灌注损伤。
Biomed Pharmacother. 2019 Mar;111:1141-1146. doi: 10.1016/j.biopha.2018.12.149. Epub 2019 Jan 12.
6
VEGF-C attenuates ischemia reperfusion injury of liver graft in rats.VEGF-C 减轻大鼠肝移植物缺血再灌注损伤。
Transpl Immunol. 2019 Jun;54:59-64. doi: 10.1016/j.trim.2019.02.004. Epub 2019 Feb 13.
7
LncRNA-MM2P Identified as a Modulator of Macrophage M2 Polarization.长链非编码 RNA-MM2P 被鉴定为巨噬细胞 M2 极化的调节剂。
Cancer Immunol Res. 2019 Feb;7(2):292-305. doi: 10.1158/2326-6066.CIR-18-0145. Epub 2018 Nov 20.
8
Activation of PPARγ by Curcumin protects mice from ischemia/reperfusion injury induced by orthotopic liver transplantation via modulating polarization of Kupffer cells.姜黄素通过调节枯否细胞极化激活 PPARγ,从而保护小鼠免受原位肝移植引起的缺血再灌注损伤。
Int Immunopharmacol. 2018 Sep;62:270-276. doi: 10.1016/j.intimp.2018.07.013. Epub 2018 Jul 23.
9
Dual Effect of Hepatic Macrophages on Liver Ischemia and Reperfusion Injury during Liver Transplantation.肝巨噬细胞在肝移植过程中对肝脏缺血再灌注损伤的双重作用
Immune Netw. 2018 Jun 28;18(3):e24. doi: 10.4110/in.2018.18.e24. eCollection 2018 Jun.
10
IRE1α aggravates ischemia reperfusion injury of fatty liver by regulating phenotypic transformation of kupffer cells.IRE1α 通过调节枯否细胞表型转化加剧肝脂肪缺血再灌注损伤。
Free Radic Biol Med. 2018 Aug 20;124:395-407. doi: 10.1016/j.freeradbiomed.2018.06.043. Epub 2018 Jun 30.