A Rapid Juvenile Murine Model of Nonalcoholic Steatohepatitis (NASH): Chronic Intermittent Hypoxia Exacerbates Western Diet-Induced NASH

Researchers designed a study to establish a rapid juvenile murine NASH model, and determined whether the combination of chronic intermittent hypoxia and a western-style diet could fully display key pathologic features of NASH.
[Life Sciences]
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Terns Announces Initiation of Dosing in Phase I Clinical Trial of TERN-501, its THR-Beta Agonist in Development for the Treatment of NASH

Terns Pharmaceuticals, Inc. announced the initiation of dosing in a Phase I clinical trial evaluating TERN-501, a selective thyroid hormone receptor beta (THR-β) agonist with high metabolic stability, enhanced liver distribution and greater selectivity for THR-β when compared with other THR-β agonists in development.
[Terns Pharmaceuticals, Inc. (Intrado GlobeNewswire LLC.)]
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Auto-Aggressive CXCR6+ CD8 T Cells Cause Liver Immune Pathology in NASH

Using a preclinical mouse model that displays key features of human nonalcoholic steatohepatitis, researchers found an indispensable role for T cells in liver immunopathology.
[Nature]
Dudek, M., Pfister, D., Donakonda, S., Filpe, P., Schneider, A., Laschinger, M., Hartmann, D., Hüser, N., Meiser, P., Bayerl, F., Inverso, D., Wigger, J., Sebode, M., Öllinger, R., Rad, R., Hegenbarth, S., Anton, M., Guillot, A., Bowman, A., … Knolle, P. A. (2021). Auto-aggressive CXCR6 + CD8 T cells cause liver immune pathology in NASH. Nature, 1–6. https://doi.org/10.1038/s41586-021-03233-8 Cite
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NASH Limits Anti-tumour Surveillance in Immunotherapy-Treated HCC

Researchers report the progressive accumulation of exhausted, unconventionally activated CD8+PD1+ T cells in non-alcoholic steatohepatitis-affected livers.
[Nature]
Pfister, D., Núñez, N. G., Pinyol, R., Govaere, O., Pinter, M., Szydlowska, M., Gupta, R., Qiu, M., Deczkowska, A., Weiner, A., Müller, F., Sinha, A., Friebel, E., Engleitner, T., Lenggenhager, D., Moncsek, A., Heide, D., Stirm, K., Kosla, J., … Heikenwalder, M. (2021). NASH limits anti-tumour surveillance in immunotherapy-treated HCC. Nature, 1–8. https://doi.org/10.1038/s41586-021-03362-0 Cite
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TIPE1 Inhibits Hepatic Steatosis, Inflammation, and Fibrosis by Suppressing Polyubiquitination of ASK1

Researchers showed that Tumor necrosis factor alpha (TNF‐α)-induced protein 8‐like 1 (TIPE1) protects against hepatic steatosis, inflammation, and fibrosis through directly binding apoptosis signal‐regulating kinase 1 (ASK1) and restraining its TNF receptor-associated factor 6‐catalyzed polyubiquitination during the development of nonalcoholic steatohepatitis.
[Hepatology]
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Inhibition of miR‐188‐5p Alleviates Hepatic Fibrosis by Significantly Reducing the Activation and Proliferation of HSCs through PTEN/PI3K/AKT Pathway

Mimicking the miR‐188‐5p resulted in the up‐regulation of hepatic stellate cell (HSC) activation and proliferation by directly targeting the phosphatase and tensin homolog (PTEN). Inhibition of miR‐188‐5p reduced the activation and proliferation markers of HSCs through PTEN/AKT pathway.
[Journal of Cellular and Molecular Medicine]
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Microbiota‐Driven Activation of Intrahepatic B Cells Aggravates Nonalcoholic Steatohepatitis through Innate and Adaptive Signaling

Scientists report that nonalcoholic steatohepatitis livers accumulate B cells with elevated pro‐inflammatory cytokine secretion and antigen‐presentation ability.
[Hepatology]
Barrow, F., Khan, S., Fredrickson, G., Wang, H., Dietsche, K., Parthiban, P., Robert, S., Kaiser, T., Winer, S., Herman, A., Adeyi, O., Mouzaki, M., Khoruts, A., Hogquist, K. A., Staley, C., Winer, D. A., & Revelo, X. S. (n.d.). Microbiota-Driven Activation of Intrahepatic B Cells Aggravates Nonalcoholic Steatohepatitis through Innate and Adaptive Signaling. Hepatology, n/a(n/a). https://doi.org/https://doi.org/10.1002/hep.31755 Cite
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Cordycepin Ameliorates Nonalcoholic Steatohepatitis via Activation of AMP‐Activated Protein Kinase Signaling Pathway

Researchers evaluated the effects of cordycepin on lipid storage in hepatocytes, inflammation, and fibrosis development in mice with nonalcoholic steatohepatitis.
[Hepatology]
Lan, T., Yu, Y., Zhang, J., Li, H., Weng, Q., Jiang, S., Tian, S., Xu, T., Hu, S., Yang, G., Zhang, Y., Wang, W., Wang, L., Zhu, Q., Rong, X., & Guo, J. (n.d.). Cordycepin Ameliorates Nonalcoholic Steatohepatitis via Activation of AMP-Activated Protein Kinase Signaling Pathway. Hepatology, n/a(n/a). https://doi.org/https://doi.org/10.1002/hep.31749 Cite
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Therapeutic Pipeline in Nonalcoholic Steatohepatitis

The authors summarize nonalcoholic steatohepatitis therapies that have progressed to Phase II and beyond. They also discuss some of the potential clinical challenges with the use of these new therapies when approved.
[Nature Reviews Gastroenterology & Hepatology]
Vuppalanchi, R., Noureddin, M., Alkhouri, N., & Sanyal, A. J. (2021). Therapeutic pipeline in nonalcoholic steatohepatitis. Nature Reviews Gastroenterology & Hepatology, 1–20. https://doi.org/10.1038/s41575-020-00408-y Cite
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The Role of Farnesoid X Receptor in Metabolic Diseases, and Gastrointestinal and Liver Cancer

Studies on the role of farnesoid X receptor in metabolic diseases and gastrointestinal and liver cancer are discussed, and the potential for development of targeted drugs are summarized.
[Nature Reviews Gastroenterology & Hepatology]
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Heterogeneity of Hepatic Stellate Cells in a Mouse Model of Non-Alcoholic Steatohepatitis (NASH)

Researchers examined the single cell expression profiles of hepatic stellate cells purified from the normal livers of foz/foz mice on a chow diet, in NASH with fibrosis of foz/foz mice on a Western diet, and in livers during regression of non‐alcoholic steatohepatitis after switching back to a chow diet.
[Hepatology]
Rosenthal, S. B., Liu, X., Ganguly, S., Dhar, D., Pasillas, M. P., Ricciardelli, E., Li, R. Z., Troutman, T. D., Kisseleva, T., Glass, C. K., & Brenner, D. A. (n.d.). Heterogeneity of hepatic stellate cells in a mouse model of non-alcoholic steatohepatitis (NASH). Hepatology, n/a(n/a). https://doi.org/https://doi.org/10.1002/hep.31743 Cite
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