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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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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Ssu72-HNF4α Signaling Axis Classify the Transition from Steatohepatitis to Hepatocellular Carcinoma

Scientists found that liver-specific deletion of Ssu72 phosphatase in mice, leads to a high incidence of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis, but not hepatocellular carcinoma.
[Cell Death & Differentiation]
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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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The Role of Hepatic Lipid Composition in Obesity-Related Metabolic Disease

Scientists summarize cross-sectional human studies using liver biopsy/lipidomics and proton magnetic resonance spectroscopy to characterize hepatic lipid composition in people with obesity and related metabolic disease.
[Liver International]
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Poxel Completes Enrollment in Phase II NASH Trial for PXL065 (DESTINY-1) in Biopsy-Proven Patients

POXEL SA announced the completion of enrollment in DESTINY-1, a dose-ranging Phase II trial evaluating PXL065 for the treatment of non-alcoholic steatohepatitis (NASH).
[POXEL SA]
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Inhibition of ATG3 Ameliorates Liver Steatosis by Increasing Mitochondrial Function

By performing a liver proteomic analysis from mice with genetic manipulation of hepatic p63, a regulator of fatty acid metabolism, investigators identified autophagy-related gene 3 (ATG3) as a new target downstream of p63.
[Journal of Hepatology]
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The Transcription Factor ZHX2 Alleviates Nonalcoholic Steatohepatitis by Transcriptional Activation of PTEN

Researchers identified a transcription factor Zinc Fingers and Homeoboxes 2 (ZHX2) in hepatocytes as a protective factor against steatohepatitis. Hepatocyte-specific ablation of ZHX2 exacerbated NASH-related phenotypes in mice, including lipid accumulation, enhanced inflammation, and hepatic fibrosis.
[Hepatology]
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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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A Human Liver Cell-Based System Modeling a Clinical Prognostic Liver Signature for Therapeutic Discovery

Researchers developed a simple and robust human liver cell-based system modeling a clinical prognostic liver signature predicting long-term liver disease progression toward hepatocellular carcinoma.
[Nature Communications]
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CohBar Granted US Patent Covering CB4211 Compositions and Use for Treating Nonalcoholic Steatohepatitis (NASH)

CohBar, Inc. announced the United States Patent and Trademark Office has granted a patent, US No. 11,111,271, covering CohBar’s lead candidate CB4211 and related compositions, as well as methods of treatment, including methods of treating NASH.
[CohBar, Inc.]
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