Therapeutic Efficacy of FASN Inhibition in Preclinical Models of HCC

The therapeutic efficacy and the molecular pathways targeted by TVB3664, either alone or with tyrosine kinase inhibitors or the checkpoint inhibitor anti-PD-L1 antibody, were assessed in human HCC cell lines and multiple oncogene-driven HCC mouse models.
[Hepatology]
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Is It Time for Chronopharmacology in NASH?

Scientists describe the potential for chronopharmacology in non-alcoholic steatohepatitis (NASH), discuss how the major NASH drug candidates are influenced by circadian biology, and encourage greater consideration of the timing of drug administration in the design of future clinical trials.
[Journal of Hepatology]
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89bio Reports Positive Topline Results from an Expansion Cohort of the Phase Ib/IIa Trial of Pegozafermin (BIO89-100) for the Treatment of NASH

89bio, Inc. announced positive topline results from an open-label expansion cohort of 20 patients in the Phase Ib/IIa proof-of-concept study evaluating pegozafermin for the treatment of non-alcoholic steatohepatitis (NASH).
[89bio, Inc.]
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Myeloid Cell TBK1 Restricts Inflammatory Responses

The authors showed that TANK-binding kinase 1 (TBK1) served as a vital regulator of proinflammatory macrophage function and protected against tissue inflammation.
[Proceedings of the National Academy of Sciences of the United States of America]
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RNF43/ZNRF3 Loss Predisposes to Hepatocellular-Carcinoma by Impairing Liver Regeneration and Altering the Liver Lipid Metabolic Ground-State

Using hepatocyte-, hepatoblast- and ductal cell-derived organoids, investigators demonstrated that the differentiation defects and lipid alterations were, in part, cell-autonomous.
[Nature Communications]
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Aligos Therapeutics Expands Collaboration with Merck to Develop Oligonucleotide Therapies for NASH

Aligos Therapeutics, Inc. announced that it has expanded its ongoing collaboration agreement with Merck to discover and develop oligonucleotide therapies for non-alcoholic steatohepatitis (NASH).
[Aligos Therapeutics, Inc.]
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An Antisense Transcript Transcribed from Irs2 Locus Contributes to the Pathogenesis of Hepatic Steatosis in Insulin Resistance

Scientists revealed a functional duality of the Irs2 gene locus, where reciprocal changes of Irs2 and ASIrs2 in obesity caused insulin resistance and steatosis.
[Cell Chemical Biology]
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The miR-23–27–24 Cluster: An Emerging Target in Nafld Pathogenesis

The authors review the current knowledge on miR-27, miR-24, and miR-23 in non-alcoholic fatty liver disease (NAFLD) pathogenesis and discuss their potential significance in NAFLD diagnosis and therapy.
[Acta Pharmacologica Sinica]
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Aligos Therapeutics Begins Dosing with NASH Drug Candidate, ALG-055009, in Healthy Volunteers in a Phase I First-in-Human Study

Aligos Therapeutics, Inc. announced that the company has started dosing in the first cohort of healthy volunteers in Study ALG-055009-301 evaluating ALG-055009 for the treatment of nonalcoholic steatohepatitis (NASH).
[Aligos Therapeutics, Inc. (Globe Newswire, Inc.)]
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The Methyltransferase METTL3 Negatively Regulates Nonalcoholic Steatohepatitis (NASH) Progression

Hepatocyte-specific deletion of Mettl3 drove nonalcoholic fatty liver-to-NASH progression by increasing CD36-mediated hepatic free fatty acid uptake and CCL2-induced inflammation, which is due to increased chromatin accessibility in the promoter region of Cd36 and Ccl2.
[Nature Communications]
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PNPLA3 Downregulation Exacerbates the Fibrotic Response in Human Hepatic Stellate Cells

Scientists characterized hepatic stellate cells obtained from patients carrying the wild type and the heterozygous or homozygous PNPLA3 I148M and investigated the effect of genotype and PNPLA3 downregulation on baseline and TGF-β-stimulated fibrotic gene expression.
[PLoS One]
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