Foresight regarding Drug Candidates Acting on the Succinate–GPR91 Signaling Pathway for Non-Alcoholic Steatohepatitis (Nash) Treatment

The authors describe the mechanism of the succinate–GPR91 signaling pathway in NASH and summarize the drugs that act on this pathway, with the aim of providing a new approach to NASH treatment.
[Biomedicine & Pharmacotherapy]
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Matrix Metalloproteinase-9 Inhibition or Deletion Attenuates Portal Hypertension in Rodents

Liver SMAD2 phosphorylation was down-regulated in all series with matrix metalloproteinase (MMP) inhibition or knock-out, and MMP-9 inhibition or deletion ameliorated the severity of cirrhosis, portal hypertension, and associated derangements.
[Journal of Cellular and Molecular Medicine]
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Targeting Epigenetically Maladapted Vascular Niche Alleviates Liver Fibrosis in Nonalcoholic Steatohepatitis

Investigators used multiomics analysis of human cirrhotic liver, a Western diet – and carbon tetrachloride – induced minipig nonalcoholic steatohepatitis model, and genetically modified mice to unravel the landscape of the vascular adaptome at the single-cell level, in which endothelial cells and TH17 cells jointly contributed to liver cirrhosis.
[Science Translational Medicine]
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Effect and Mechanism of Vitamin D Activation Disorder on Liver Fibrosis in Biliary Atresia

Researchers investigated the effect of differential expression of CYP2R1 in hepatocytes on the expression of genes related to liver fibrosis in primary hepatic stellate cells of biliary atresia and animal models of cholestasis.
[Scientific Reports]
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Single-Cell and Bulk Transcriptomics of the Liver Reveals Potential Targets of NASH with Fibrosis

Scientists profiled 17,810 non-parenchymal cells derived from six healthy human livers, which enabled the identification of potential intercellular signaling axes and master regulators responsible for the activation of hepatic stellate cells during fibrogenesis.
[Scientific Reports]
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O-GlcNAcylation Inhibits Hepatic Stellate Cell Activation

The authors aimed to evaluate the role of O-GlcNAc transferase (OGT) in hepatic stellate cells (HSCs) and its consequent role in liver fibrosis. RNA-seq showed that OGT knockdown in HSCs modulated key signaling pathways involved in HSC activation.
[Journal of Gastroenterology and Hepatology]
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Blade Therapeutics Announces Positive Data from Preclinical Drug-Drug Interaction Study of Cudetaxestat, a Non-Competitive Autotaxin Inhibitor in Clinical Development for Idiopathic Pulmonary Fibrosis (IPF)

Blade Therapeutics, Inc., a biopharmaceutical company focused on developing cutting-edge treatments for fibrotic and neurodegenerative diseases, announced positive preliminary data from a new preclinical study of cudetaxestat, an investigational non-competitive autotaxin inhibitor in clinical development for IPF.
[Blade Therapeutics, Inc.]
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Conditioned Medium from Stem Cells Derived from Human Exfoliated Deciduous Teeth Ameliorates NASH via the Gut-Liver Axis

The authors examined the benefits of serum-free conditioned medium from stem cells derived from human exfoliated deciduous teeth on a murine non-alcoholic steatohepatitis (NASH) model induced by a combination of Western diet and repeated administration of low doses of carbon tetrachloride intraperitoneally, focusing on the gut-liver axis.
[Scientific Reports]
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Effect of HGF-Transfected Human Umbilical Cord Mesenchymal Stem Cells on Hepatic Stellate Cells by Regulating TGF-β1/Smads Signaling Pathway

Investigators explored the possible mechanism of HGF-transfected human umbilical cord MSCs in inhibiting the proliferation and activation of hepatic stellate cells-T6.
[Stem Cells and Development]
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miR-139-5p Sponged by LncRNA NEAT1 Regulates Liver Fibrosis via Targeting β-Catenin/SOX9/TGF-β1 Pathway

Scientists demonstrated that the expression of lncRNA NEAT1 was increased and the expression of miR-139-5p was decreased in fibrotic liver tissues. LncRNA NEAT1 could sponge miR-139-5p and promoted hepatic stellate cells activation by directly inhibiting the expression of miR-139-5p.
[Cell Death Discovery]
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Targeting Integrin αvβ3 by a Rationally Designed Protein for Chronic Liver Disease Treatment

The authors reported a strategy for chronic liver disease treatment by induction of integrin αvβ3 mediated cell apoptosis using a rationally designed protein (ProAgio). ProAgio was designed to target integrin αvβ3 at a novel site, which was highly expressed in activated hepatic stellate cells, angiogenic endothelium, and capillarized liver sinusoidal endothelial cells.
[Communications Biology]
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