Research Progress on the Association Between PU.1 and Liver Fibrosis
Journal: Journal of Clinical Medicine Research DOI: 10.32629/jcmr.v6i1.3724
Abstract
Liver fibrosis is a pathophysiological process characterized by excessive proliferation of intrahepatic connective tissue induced by chronic hepatic injury. Its molecular mechanisms include inflammation-mediated macrophage activation, hepatic stellate cell activation, and various fibrogenic pathways. Early fibrosis is reversible, which is why early diagnosis and treatment are essential.The emerging evidence underlines the importance of the transcription factor PU.1 in liver fibrosis development. This review is done to relate PU.1 with liver fibrosis for diagnosis and therapy insight into the condition.
Keywords
liver fibrosis, PU.1, hepatic macrophages, hepatic stellate cells, signaling pathways
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[15] Etzrodt M, Ahmed N, Hoppe P S, et al. Inflammatory signals directly instruct PU.1 in HSCs via TNF[J]. Blood, 2019, 133(8): 816-819.
[16] Zhang Z, Yuan Y, Hu L, et al. ANGPTL8 accelerates liver fibrosis mediated by HFD-induced inflammatory activity via LILRB2/ERK signaling pathways[J]. Journal of Advanced Research, 2023, 47: 41-56.
[2] Sa T, Rp D. The transcription factor PU.1 is a critical regulator of cellular communication in the immune system[J]. Archivum immunologiae et therapiae experimentalis, 2011, 59(6).
[3] T W, S R, S U, et al. PU.1 controls fibroblast polarization and tissue fibrosis[J]. Nature, 2019, 566(7744).
[4] Bernard N J. PU.1 pulls the strings in fibrotic disease[J]. Nature Reviews Rheumatology, 2019, 15(4): 187-187.
[5] Hu J, Zhang J J, Li L, et al. PU.1 inhibition attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II by reducing TGF-β1/Smads pathway activation[J]. Journal of Cellular and Molecular Medicine, 2021, 25(14): 6746-6759.
[6] Bonnardel J, T’Jonck W, Gaublomme D, et al. Stellate Cells, Hepatocytes, and Endothelial Cells Imprint the Kupffer Cell Identity on Monocytes Colonizing the Liver Macrophage Niche[J]. Immunity, 2019, 51(4): 638-654.e9.
[7] Wang Z, Du K, Jin N, et al. Macrophage in liver Fibrosis: Identities and mechanisms[J]. International Immunopharmacology, 2023, 120: 110357.
[8] Karpurapu M, Wang X, Deng J, et al. Functional PU.1 in macrophages has a pivotal role in NF-κB activation and neutrophilic lung inflammation during endotoxemia[J]. Blood, 2011, 118(19): 5255-5266.
[9] Liu Q, Yu J, Wang L, et al. Inhibition of PU.1 ameliorates metabolic dysfunction and non-alcoholic steatohepatitis[J]. Journal of Hepatology, 2020, 73(2): 361-370.
[10] Zhang C Y, Yuan W G, He P, et al. Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets[J]. World Journal of Gastroenterology, 2016, 22(48): 10512-10522.
[11] Liu Q, Zhang Y, Yang S, et al. PU.1-deficient mice are resistant to thioacetamide-induced hepatic fibrosis: PU.1 finely regulates Sirt1 expression via transcriptional promotion of miR-34a and miR-29c in hepatic stellate cells[J]. Bioscience Reports, 2017, 37(6): BSR20170926.
[12] Ji G, Zhang Z, Wang X, et al. Comprehensive evaluation of the mechanism of human adipose mesenchymal stem cells ameliorating liver fibrosis by transcriptomics and metabolomics analysis[J]. Scientific Reports, 2024, 14(1): 20035.
[13] B D, C M, S D, et al. TGF-β in Hepatic Stellate Cell Activation and Liver Fibrogenesis-Updated 2019[J]. Cells, 2019, 8(11).
[14] Poulsen K L, Ross C K C D, Chaney J K, et al. Role of the chemokine system in liver fibrosis: a narrative review[J]. Digestive Medicine Research, 2022, 5(0).
[15] Etzrodt M, Ahmed N, Hoppe P S, et al. Inflammatory signals directly instruct PU.1 in HSCs via TNF[J]. Blood, 2019, 133(8): 816-819.
[16] Zhang Z, Yuan Y, Hu L, et al. ANGPTL8 accelerates liver fibrosis mediated by HFD-induced inflammatory activity via LILRB2/ERK signaling pathways[J]. Journal of Advanced Research, 2023, 47: 41-56.
Copyright © 2025 Honglin Ju, Qian Li, Siqi Cheng, Ya Liu, Li Yang
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