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hepatic stellate cells

Parthenolide, Bioactive Compound of Chrysanthemum parthenium L., Ameliorates Fibrogenesis and Inflammation in Hepatic Fibrosis via Regulating the Crosstalk of TLR4 and STAT3 Signaling Pathway

[Phytotherapy Research] Scientists focused on the regulatory effects of parthenolide, a bioactive component derived from Chrysanthemum parthenium L., against hepatic fibrosis via regulating the crosstalk of toll-like receptor 4 and signal transducer and activator of transcription 3 in activated hepatic stellate cells.

Roles of Nuclear Receptors in Hepatic Stellate Cells

[Expert Review of Gastroenterology & Hepatology] The authors summarized the recent progress in the understanding of the regulatory role of nuclear receptors in hepatic stellate cells and their potential as drug targets in liver fibrosis.

Periostin Deficiency Reduces DEN-Induced Liver Cancer in Mice by Decreasing HSC Activation and Cancer Cell Proliferation

[Journal of Pathology] Scientists demonstrated that periostin was markedly upregulated in diethylnitrosamine (DEN)-induced mouse hepatocellular carcinoma tissues (HCC) and periostin knockout impaired DEN-induced HCC development.

C/EBP-α Induces Autophagy by Binding to Beclin1 through Its Own Acetylation Modification in Activated Hepatic Stellate Cells

[Experimental Cell Research] Scientists characterized the consequence of CCAAT/enhancer binding protein α overexpression on the expression of proteins LC3B, P62, ATG5 and Beclin1 which were related to autophagy in hepatic stellate cells.

Exosomes Secreted by Palmitic Acid-Treated Hepatocytes Promote LX-2 Cell Activation by Transferring miRNA-107

[Cell Death Discovery] Scientists explored the role of exosomes derived from palmitic acid -treated hepatocytes in regulating hepatic stellate cells (LX-2 cell) proliferation and activation and the underlying mechanisms.

Liver-Fibrosis-Activated Transcriptional Networks Govern Hepatocyte Reprogramming and Intra-hepatic Communication

[Cell Metabolism] Using cell-type-resolved genomics, scientists showed that comprehensive alterations in hepatocyte genomic and transcriptional settings during non-alcoholic steatohepatitis progression, led to a loss of hepatocyte identity.

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