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Cdc42 is crucial for the early regulation of hepatic stellate cell activation.
Am J Physiol Cell Physiol
January 2025
Department of Anatomy and Regenerative Biology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
The activation of hepatic stellate cells (HSCs) from a quiescent state is a cause of liver fibrosis and a therapeutic target. HSCs are resident mesenchymal cells located in the space of Disse, exhibiting specialized morphological characteristics such as a stellate shape, large lipid droplets, and direct adhesions to hepatocytes via microprojections called HSC spines. Morphological alterations in HSCs play a crucial role in initiating their activation.
View Article and Find Full Text PDFThe adiponectin-PPARγ axis in hepatic stellate cells regulates liver fibrosis.
Cell Rep
January 2025
Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address:
Hepatic stellate cells (HSCs) are key drivers of local fibrosis. Adiponectin, conventionally thought of as an adipokine, is also expressed in quiescent HSCs. However, the impact of its local expression on the progression of liver fibrosis remains unclear.
View Article and Find Full Text PDFUlcerative Colitis Preceding Asymptomatic Wilson's Disease: A Case Report and Literature Review.
Gastro Hep Adv
September 2024
Department of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo, Japan.
An 11-year-old girl with quiescent ulcerative colitis had sustained elevation of liver enzymes. Although she had no clinical symptoms suggestive of Wilson's disease, such as Kayser-Fleischer rings, laboratory data showed decreased serum copper and ceruloplasmin levels and increased urinary copper excretion. Genetic testing showed pathogenic variants in allele 1: c.
View Article and Find Full Text PDFHepatic stellate cell single cell atlas reveals a highly similar activation process across liver disease aetiologies.
JHEP Rep
January 2025
Vrije Universiteit Brussel, Liver Cell Biology research group, Laarbeeklaan 103, 1090 Brussel, Belgium.
Article Synopsis
- This research explores the activation of hepatic stellate cells (HSCs) across different types of chronic liver disease (CLD), finding that their activation follows similar mechanisms regardless of the injury type.
- A single-cell RNA-sequencing atlas was created to categorize HSCs into three profiles: quiescent, initiatory, and myofibroblasts, indicating consistent activation patterns in both mice and humans.
- The study highlights key transcription factors and novel ligands involved in HSC activation, paving the way for new insights and potential treatments for liver fibrosis.
In Vivo Selection of S/MAR Sequences to Favour AAV Episomal Maintenance in Dividing Cells.
Int J Mol Sci
November 2024
Vivet Therapeutics S.L., 31008 Pamplona, Spain.
Adeno-associated viral (AAV) vector-mediated gene therapy has emerged as a promising alternative to liver transplantation for monogenic metabolic hepatic diseases. AAVs are non-integrative vectors that are maintained primarily as episomes in quiescent cells like adult hepatocytes. This quality, while advantageous from a safety perspective due to a decreased risk of insertional mutagenesis, becomes a disadvantage when treating dividing cells, as it inevitably leads to the loss of the therapeutic genome.
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