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巨噬细胞极化在肝纤维化中的调控作用机制

白小洋 张旭 海龙 丁向春

引用本文:
Citation:

巨噬细胞极化在肝纤维化中的调控作用机制

DOI: 10.12449/JCH240329
基金项目: 

宁夏自然科学基金项目 (2023AAC03584);

宁夏自然科学基金项目 (2023AAC03519)

利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:白小洋负责撰写与修改论文;海龙参与查阅相关文献;丁向春、张旭负责拟定写作思路,指导撰写文章并最后定稿。
详细信息
    通信作者:

    丁向春, 13619511758@163.com (ORCID: 0000-0003-0283-9419)

Regulatory effect and mechanism of macrophage polarization in liver fibrosis

Research funding: 

Ningxia Natural Science Foundation (2023AAC03584);

Ningxia Natural Science Foundation (2023AAC03519)

More Information
    Corresponding author: DING Xiangchun, 13619511758@163.com (ORCID: 0000-0003-0283-9419)
  • 摘要: 肝纤维化是一种由病毒感染、酒精、化学物质等原因导致的慢性肝损伤的愈合反应,是慢性肝脏疾病进展为肝硬化和肝癌的关键环节。肝巨噬细胞被认为是肝损伤和修复的重要介质,巨噬细胞极化趋向对肝纤维化具有双向调控作用。本文阐述不同表型的肝巨噬细胞在肝纤维化发生发展过程中的作用,以期为纤维化的防治研究提供新思路。

     

  • 图  1  巨噬细胞极化在肝纤维化中的调控作用机制

    Figure  1.  The regulatory mechanism of macrophage polarization in liver fibrosis

  • [1] KOYAMA Y, BRENNER DA. Liver inflammation and fibrosis[J]. J Clin Invest, 2017, 127( 1): 55- 64. DOI: 10.1172/JCI88881.
    [2] LIU M, HU Y, YUAN Y, et al. γδT cells suppress liver fibrosis via strong cytolysis and enhanced NK cell-mediated cytotoxicity against hepatic stellate cells[J]. Front Immunol, 2019, 10: 477. DOI: 10.3389/fimmu.2019.00477.
    [3] KRENKEL O, TACKE F. Liver macrophages in tissue homeostasis and disease[J]. Nat Rev Immunol, 2017, 17( 5): 306- 321. DOI: 10.1038/nri.2017.11.
    [4] SICA A, MANTOVANI A. Macrophage plasticity and polarization: in vivo veritas[J]. J Clin Invest, 2012, 122( 3): 787- 795. DOI: 10.1172/JCI59643.
    [5] SHAPOURI-MOGHADDAM A, MOHAMMADIAN S, VAZINI H, et al. Macrophage plasticity, polarization, and function in health and disease[J]. J Cell Physiol, 2018, 233( 9): 6425- 6440. DOI: 10.1002/jcp.26429.
    [6] WANG L, ZHANG H, SUN L, et al. Manipulation of macrophage polarization by peptide-coated gold nanoparticles and its protective effects on acute lung injury[J]. J Nanobiotechnology, 2020, 18( 1): 38. DOI: 10.1186/s12951-020-00593-7.
    [7] XU F, GUO M, HUANG W, et al. Annexin A5 regulates hepatic macrophage polarization via directly targeting PKM2 and ameliorates NASH[J]. Redox Biol, 2020, 36: 101634. DOI: 10.1016/j.redox.2020.101634.
    [8] ZHAO S, MI Y, GUAN B, et al. Tumor-derived exosomal miR-934 induces macrophage M2 polarization to promote liver metastasis of colorectal cancer[J]. J Hematol Oncol, 2020, 13( 1): 156. DOI: 10.1186/s13045-020-00991-2.
    [9] MA PF, GAO CC, YI J, et al. Cytotherapy with M1-polarized macrophages ameliorates liver fibrosis by modulating immune microenvironment in mice[J]. J Hepatol, 2017, 67( 4): 770- 779. DOI: 10.1016/j.jhep.2017.05.022.
    [10] YANG Y, YE YC, CHEN Y, et al. Crosstalk between hepatic tumor cells and macrophages via Wnt/β-catenin signaling promotes M2-like macrophage polarization and reinforces tumor malignant behaviors[J]. Cell Death Dis, 2018, 9( 8): 793. DOI: 10.1038/s41419-018-0818-0.
    [11] KAZANKOV K, JØRGENSEN S, THOMSEN KL, et al. The role of macrophages in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis[J]. Nat Rev Gastroenterol Hepatol, 2019, 16( 3): 145- 159. DOI: 10.1038/s41575-018-0082-x.
    [12] van der HEIDE D, WEISKIRCHEN R, BANSAL R. Therapeutic targeting of hepatic macrophages for the treatment of liver diseases[J]. Front Immunol, 2019, 10: 2852. DOI: 10.3389/fimmu.2019.02852.
    [13] KRENKEL O, TACKE F. Liver macrophages in tissue homeostasis and disease[J]. Nat Rev Immunol, 2017, 17( 5): 306- 321. DOI: 10.1038/nri.2017.11.
    [14] MATSUDA M, SEKI E. Hepatic stellate cell-macrophage crosstalk in liver fibrosis and carcinogenesis[J]. Semin Liver Dis, 2020, 40( 3): 307- 320. DOI: 10.1055/s-0040-1708876.
    [15] SINGLA RD, WANG J, SINGLA DK. Regulation of Notch 1 signaling in THP-1 cells enhances M2 macrophage differentiation[J]. Am J Physiol Heart Circ Physiol, 2014, 307( 11): H1634- H1642. DOI: 10.1152/ajpheart.00896.2013.
    [16] WEI W, LI ZP, BIAN ZX, et al. Astragalus polysaccharide RAP induces macrophage phenotype polarization to M1 via the Notch signaling pathway[J]. Molecules, 2019, 24( 10): 2016. DOI: 10.3390/molecules24102016.
    [17] ZHENG S, ZHANG P, CHEN Y, et al. Inhibition of Notch signaling attenuates schistosomiasis hepatic fibrosis via blocking macrophage M2 polarization[J]. PLoS One, 2016, 11( 11): e0166808. DOI: 10.1371/journal.pone.0166808.
    [18] TRAVIS MA, SHEPPARD D. TGF-β activation and function in immunity[J]. Annu Rev Immunol, 2014, 32: 51- 82. DOI: 10.1146/annurev-immunol-032713-120257.
    [19] LU H, WU L, LIU L, et al. Quercetin ameliorates kidney injury and fibrosis by modulating M1/M2 macrophage polarization[J]. Biochem Pharmacol, 2018, 154: 203- 212. DOI: 10.1016/j.bcp.2018.05.007.
    [20] CHEN B, HUANG S, SU Y, et al. Macrophage Smad3 protects the infarcted heart, stimulating phagocytosis and regulating inflammation[J]. Circ Res, 2019, 125( 1): 55- 70. DOI: 10.1161/CIRCRESAHA.119.315069.
    [21] XIN P, XU X, DENG C, et al. The role of JAK/STAT signaling pathway and its inhibitors in diseases[J]. Int Immunopharmacol, 2020, 80: 106210. DOI: 10.1016/j.intimp.2020.106210.
    [22] WANG F, ZHANG S, JEON R, et al. Interferon gamma induces reversible metabolic reprogramming of M1 macrophages to sustain cell viability and pro-inflammatory activity[J]. EBioMedicine, 2018, 30: 303- 316. DOI: 10.1016/j.ebiom.2018.02.009.
    [23] HU X, CHEN J, WANG L, et al. Crosstalk among Jak-STAT, Toll-like receptor, and ITAM-dependent pathways in macrophage activation[J]. J Leukoc Biol, 2007, 82( 2): 237- 243. DOI: 10.1189/jlb.1206763.
    [24] HE Y, GAO Y, ZHANG Q, et al. IL-4 switches microglia/macrophage M1/M2 polarization and alleviates neurological damage by modulating the JAK1/STAT6 pathway following ICH[J]. Neuroscience, 2020, 437: 161- 171. DOI: 10.1016/j.neuroscience.2020.03.008.
    [25] GAO S, ZHOU J, LIU N, et al. Curcumin induces M2 macrophage polarization by secretion IL-4 and/or IL-13[J]. J Mol Cell Cardiol, 2015, 85: 131- 139. DOI: 10.1016/j.yjmcc.2015.04.025.
    [26] QUERO L, TIADEN AN, HANSER E, et al. miR-221-3p drives the shift of M2-macrophages to a pro-inflammatory function by suppressing JAK3/STAT3 activation[J]. Front Immunol, 2019, 10: 3087. DOI: 10.3389/fimmu.2019.03087.
    [27] QIAN M, WANG S, GUO X, et al. Hypoxic glioma-derived exosomes deliver microRNA-1246 to induce M2 macrophage polarization by targeting TERF2IP via the STAT3 and NF-‍κB pathways[J]. Oncogene, 2020, 39( 2): 428- 442. DOI: 10.1038/s41388-019-0996-y.
    [28] BAO L, LI X. MicroRNA-32 targeting PTEN enhances M2 macrophage polarization in the glioma microenvironment and further promotes the progression of glioma[J]. Mol Cell Biochem, 2019, 460( 1-2): 67- 79. DOI: 10.1007/s11010-019-03571-2.
    [29] HU J, HUANG CX, RAO PP, et al. Inhibition of microRNA-155 attenuates sympathetic neural remodeling following myocardial infarction via reducing M1 macrophage polarization and inflammatory responses in mice[J]. Eur J Pharmacol, 2019, 851: 122- 132. DOI: 10.1016/j.ejphar.2019.02.001.
    [30] DHAR D, BAGLIERI J, KISSELEVA T, et al. Mechanisms of liver fibrosis and its role in liver cancer[J]. Exp Biol Med(Maywood), 2020, 245( 2): 96- 108. DOI: 10.1177/1535370219898141.
    [31] PRADERE JP, KLUWE J, de MINICIS S, et al. Hepatic macrophages but not dendritic cells contribute to liver fibrosis by promoting the survival of activated hepatic stellate cells in mice[J]. Hepatology, 2013, 58( 4): 1461- 1473. DOI: 10.1002/hep.26429.
    [32] KISSELEVA T, BRENNER D. Molecular and cellular mechanisms of liver fibrosis and its regression[J]. Nat Rev Gastroenterol Hepatol, 2021, 18( 3): 151- 166. DOI: 10.1038/s41575-020-00372-7.
    [33] BANSAL R, van BAARLEN J, STORM G, et al. The interplay of the Notch signaling in hepatic stellate cells and macrophages determines the fate of liver fibrogenesis[J]. Sci Rep, 2015, 5: 18272. DOI: 10.1038/srep18272.
    [34] WATANABE Y, TSUCHIYA A, SEINO S, et al. Mesenchymal stem cells and induced bone marrow-derived macrophages synergistically improve liver fibrosis in mice[J]. Stem Cells Transl Med, 2019, 8( 3): 271- 284. DOI: 10.1002/sctm.18-0105.
    [35] LUO XY, MENG XJ, CAO DC, et al. Transplantation of bone marrow mesenchymal stromal cells attenuates liver fibrosis in mice by regulating macrophage subtypes[J]. Stem Cell Res Ther, 2019, 10( 1): 16. DOI: 10.1186/s13287-018-1122-8.
    [36] WANG M, ZHANG M, FU L, et al. Liver-targeted delivery of TSG-6 by calcium phosphate nanoparticles for the management of liver fibrosis[J]. Theranostics, 2020, 10( 1): 36- 49. DOI: 10.7150/thno.37301.
    [37] SONG WJ, LI Q, MO RYU, et al. TSG-6 released from intraperitoneally injected canine adipose tissue-derived mesenchymal stem cells ameliorate inflammatory bowel disease by inducing M2 macrophage switch in mice[J]. Stem Cell Res Ther, 2018, 9( 1): 91. DOI: 10.1186/s13287-018-0841-1.
    [38] TOSELLO-TRAMPONT AC, KRUEGER P, NARAYANAN S, et al. NKp46(+) natural killer cells attenuate metabolism-induced hepatic fibrosis by regulating macrophage activation in mice[J]. Hepatology, 2016, 63( 3): 799- 812. DOI: 10.1002/hep.28389.
    [39] YUNNA C, MENGRU H, LEI W, et al. Macrophage M1/M2 polarization[J]. Eur J Pharmacol, 2020, 877: 173090. DOI: 10.1016/j.ejphar.2020.173090.
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出版历程
  • 收稿日期:  2023-08-10
  • 录用日期:  2023-11-10
  • 出版日期:  2024-03-20
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