IL-1α was sufficient to activate cultured fibroblasts and primary hepatic stellate cells in vitro, and IL-1α was elevated in the sera and liver of cachectic, suggesting a mechanism by which chronic IL-1R signaling could be leading to cachexia-associated fibrosis.
TREM-2 expression was analysed in liver tissues of two independent cohorts of patients with hepatocellular carcinoma (HCC) and compared with control liver samples. Experimental HCC and liver regeneration models in wild type and Trem-2-/- mice, and in vitro studies with hepatic stellate cells and HCC spheroids were conducted.
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Esparza-Baquer, A., Labiano, I., Sharif, O., Agirre-Lizaso, A., Oakley, F., Rodrigues, P. M., Zhuravleva, E., O’Rourke, C. J., Hijona, E., Jimenez-Agüero, R., Riaño, I., Landa, A., Casta, A. L., Zaki, M. Y. W., Munoz-Garrido, P., Azkargorta, M., Elortza, F., Vogel, A., Schabbauer, G., … Perugorria, M. J. (2020). TREM-2 defends the liver against hepatocellular carcinoma through multifactorial protective mechanisms. Gut. https://doi.org/10.1136/gutjnl-2019-319227 Cite
Diseases like non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) bring a very high level of pathogenic complexity and far-reaching implications that apply not only scientists but also to clinicians, patients, regulators, bio-pharmaceutical industry and third-party payers.
[Journal of Hepatology]
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Researchers elucidated the anti-fibrotic effects of neratinib in hepatic stellate cells (HSCs) and in vivo models of CCl4-induced liver fibrosis. HSC activation was a key step in liver fibrogenesis and played a crucial role in collagen deposition, as it is primarily responsible for excessive ECM production.
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Park, Y. J., An, H.-T., Park, J.-S., Park, O., Duh, A. J., Kim, K., Chung, K. H., Lee, K. C., Oh, Y., & Lee, S. (2020). Tyrosine kinase inhibitor neratinib attenuates liver fibrosis by targeting activated hepatic stellate cells. Scientific Reports, 10(1), 14756. https://doi.org/10.1038/s41598-020-71688-2 Cite
Scientists investigated the effect of human fetal skin-derived stem cell (hFSSC) secretome in the treatment of liver fibrosis. They investigated the anti-fibrotic mechanism of hFSSC secretome in hepatic stellate cells.
[Stem Cell Research & Therapy]
This review explores the causes and mechanisms of hepatic fibrosis and focuses on the roles of key molecules involved in liver fibro genesis, some of which are potential targets for therapeutics to hamper liver fibro genesis.
[Journal of Interferon and Cytokine Research]
Scientists investigated the effect of leptin on the expression of Mat2b in hepatic stellate cells in vitro and in a leptin‐deficient mouse model. Results demonstrated that leptin significantly increased Mat2b expression.
[Journal of Pathology]
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Researchers demonstrated that primary mouse and human hepatocytes can undergo pyroptosis upon NLRP3 inflammasome activation with subsequent release of NLRP3 inflammasome proteins that amplified and perpetuated inflammasome-driven fibrogenesis.
[Journal of Hepatology]
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Gaul, S., Leszczynska, A., Alegre, F., Kaufmann, B., Johnson, C. D., Adams, L. A., Wree, A., Damm, G., Seehofer, D., Calvente, C. J., Povero, D., Kisseleva, T., Eguchi, A., McGeough, M. D., Hoffman, H. M., Pelegrin, P., Laufs, U., & Feldstein, A. E. (2020). Hepatocyte pyroptosis and release of inflammasome particles induce stellate cell activation and liver fibrosis. Journal of Hepatology, 0(0). https://doi.org/10.1016/j.jhep.2020.07.041 Cite
Wild‐type, KitW‐sh, and Mdr2‐/‐ mice lacking l‐histidine decarboxylase were injected with vehicle or PKH26‐tagged murine mast cells pretreated with 0.01% DMSO or the TGF‐βR inhibitor,
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A coculture system and a subcutaneous xenograft model involving coimplantation of mouse hepatoma cells and primary activated hepatic stellate cells were used to study the effects of dexmedetomidine on hepatocellular carcinoma progression.
[Experimental and Molecular Medicine]
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Chen, P., Luo, X., Dai, G., Jiang, Y., Luo, Y., Peng, S., Wang, H., Xie, P., Qu, C., Lin, W., Hong, J., Ning, X., & Li, A. (2020). Dexmedetomidine promotes the progression of hepatocellular carcinoma through hepatic stellate cell activation. Experimental & Molecular Medicine, 1–13. https://doi.org/10.1038/s12276-020-0461-6 Cite
While no major difference was observed after bile duct ligation or 3,5-diethoxycarbonyl-1,4-dihydrocollidine, platelet-derived growth factor receptor α loss in hepatic stellate cells (HSCs) led to a significant albeit transient reduction in fibrosis after CCl4 injury, associated with increased HSC death and reduced migration.
[American Journal of Pathology]
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