[1] Kisseleva T, Brenner D. Molecular and cellular mechanisms of liver fibrosis and its regression[J].Nat Rev Gastroenterol Hepatol,2020,18(3):151-166.
[2] Campana L,Iredale J P. Regression of liver fibrosis[J].Semin Liver Dis,2017,37(1):1-10.
[3] 陶山,李倩,陈阳,等.肝巨噬细胞与肝星状细胞交互作用对肝纤维化发生与逆转的影响[J].生命科学,2021,33(3):363-373.
[4] Wen Y,Lambrecht J,Ju C, et al. Hepatic macrophages in liver homeostasis and diseases-diversity, plasticity and therapeutic opportunities[J]. Cell Mol Immunol,2021,18(1):45-56.
[5] Matsuda M, Seki E. Hepatic stellate cell-macrophage crosstalk in liver fibrosis and carcinogenesis[J]. Semin Liver Dis,2020,40(3):307-320.
[6] Shapouri-Moghaddam A, Mohammadian S, Vazini H, et al. Macrophage plasticity, polarization, and function in health and disease[J].Cell Physiol,2018,233(9):6425-6440.
[7] 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].Nanobiotechnology,2020,18(1):38.
[8] Xu F,Guo M,Huang W,et al. Annexin A5 regulates hepatic macrophage polarization via directly targeting PKM2 and ameliorates NASH[J].Redox Biology,2020,36:101634.
[9] 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].Hematol Oncol,2020,13(1):156-156.
[10] Ma P,Gao C,Yi J,et al. Cytotherapy with M1-polarized macrophages ameliorates liver fibrosis by modulating immune microenvironment in mice[J].Hepatol,2017,67(4):770-779.
[11] Yang Y,Ye Y,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):1-14.
[12] Kazankov K, Jørgensen S M D, Thomsen K L,et al. The role of macrophages in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis[J].Nat Rev Gastroenterol Hepatol,2019,16(3):145-159.
[13] 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.
[14] Krenkel O, Tacke F. Liver macrophages in tissue homeostasis and disease[J].Nat Rev Immunol,2017,17(5):306-321.
[15] Matsuda M, Seki E. Hepatic stellate cell-macrophage crosstalk in liver fibrosis and carcinogenesis[J]. Semin Liver Dis,2020,40(3):307-320.
[16] Gong J, Li J, Dong H, et al. Inhibitory effects of berberine on proinflammatory M1 macrophage polarization through interfering with the interaction between TLR4 and MyD88[J].BMC Complement Altern Med,2019,19(1):314.
[17] 徐俊,戚璐,许杰,等. 基于TLR4/MyD88/NF-κB信号通路探讨抗纤软肝方抗肝纤维化的实验研究[J].时珍国医国药,2020,31(12):2908-2911.
[18] Siebel C, Lendahl U. Notch signaling in development, tissue homeostasis, and disease[J].Physiol Rev, 2017,97(4):1235-1294.
[19] Keewan E,Naser S A. The role of notch signaling in macrophages during inflammation and infection: implication in rheumatoid arthritis?[J].Cells,2020,9(1):111.
[20] Shanaki M,Khosravi M,Khoshdooni-Farahani A,et al. High-intensity interval training reversed high-fat diet–induced m1-macrophage polarization in rat adipose tissue via inhibition of NOTCH signaling[J].J Inflamm Res,2020,2020(default):165-174.
[21] Hu X, Hong B, Shan X, et al. The effect of poria cocos polysaccharide PCP-1C on M1 macrophage polarization via the notch signaling pathway[J].Molecules,2023,28(5):2140.
[22] 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.
[23] 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.
[24] Quero L, Tiaden A N, 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.
[25] Liu P,Li H,Gong J S,et al. Chitooligosaccharides alleviate hepatic fibrosis by regulating the polarization of M1 and M2 macrophages[J].Food Funct,2022,13(2):753-768.
[26] Zhao M, Wang L, Wang M, et al. Targeting fibrosis, mechanisms and cilinical trials[J].Signal Transduct Target Ther,2022,7(1):206.
[27] 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.
[28] Fang W,Deng Z,Benadjaoud F,et al. Cathepsin B deficiency ameliorates liver lipid deposition, inflammatory cell infiltration, and fibrosis after diet-induced nonalcoholic steatohepatitis[J].Transl Res, 2020,222:28-40.
[29] Koyama Y,Brenner D A. Liver inflammation and fibrosis[J].J Clin Invest,2017,127(1):55-64.
[30] Yunna C,Mengru H,Lei W,et al. Macrophage M1/M2 polarization[J].Eur J Pharmacol,2020,877:173090.
[31] Bartneck M,Koppe C,Fech V,et al. Roles of CCR2 and CCR5 for hepatic macrophage polarization in mice with liver parenchymal cell-specific NEMO deletion[J].Cell Mol Gastroenterol Hepatol,2021,11(2):327-347.
[32] 彭望霞,陆华冠,谢新,等.巨噬细胞极化在肝纤维化中的作用和调控机制以及中国传统医药的干预[J].中国新药杂志,2024,33(10):1021-1031. |
