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liver fibrosis

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

[Biomedicine & Pharmacotherapy] 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.

Matrix Metalloproteinase-9 Inhibition or Deletion Attenuates Portal Hypertension in Rodents

[Journal of Cellular and Molecular Medicine] 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.

Targeting Epigenetically Maladapted Vascular Niche Alleviates Liver Fibrosis in Nonalcoholic Steatohepatitis

[Science Translational Medicine] 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.

Effect and Mechanism of Vitamin D Activation Disorder on Liver Fibrosis in Biliary Atresia

[Scientific Reports] 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.

Single-Cell and Bulk Transcriptomics of the Liver Reveals Potential Targets of NASH with Fibrosis

[Scientific Reports] 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.

O-GlcNAcylation Inhibits Hepatic Stellate Cell Activation

[Journal of Gastroenterology and Hepatology] 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.

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