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hepatic stellate cells

Hepcidin in Hepatocellular Carcinoma

[British Journal of Cancer] The authors explore hepcidin in HCC, presenting the levels of tissue and serum hepcidin and explaining the mechanisms that contribute to hepcidin reduction in HCC.

Fibroblast Growth Factor 18 Attenuates Liver Fibrosis and HSCs Activation via the SMO-LATS1-YAP Pathway

[Pharmacological Research] Scientists found that fibroblast growth factor 18 was markedly upregulated in carbon tetrachloride-induced fibrotic mouse liver tissues and transforming growth factor β stimulated LX-2 cells.

Mimicking Native Liver Lobule Microarchitecture In Vitro with Parenchymal and Non-Parenchymal Cells Using 3D Bioprinting for Drug Toxicity and Drug Screening Applications

[ACS Applied Materials & interfaces] A physiologically relevant human vascularized liver model was bioprinted with a novel liver extracellular matrix-based bioink laden with human adipose mesenchymal stem cell-derived hepatocyte-like cells, human umbilical vein endothelial cells, and human hepatic stellate cells.

Growth Hormone and Insulin-Like Growth Factor I Regulation of Nonalcoholic Fatty Liver Disease

[Journal of Clinical Endocrinology & Metabolism] Investigators focus on the potential role of growth hormone and insulin-like growth factor I in the regulation of hepatic steatosis, inflammation, and fibrosis.

ECM1 Modified HF-MSCs Targeting HSC Attenuate Liver Cirrhosis by Inhibiting the TGF-β/Smad Signaling Pathway

[Cell Death Discovery] To improve the effectiveness of naïve hair follicle-derived-MSC (HF-MSC) treatments on liver cirrhosis (LC), the authors used bioinformatic tools to identify an exogenous gene targeting hepatic stellate cells (HSCs) among the differentially expressed genes in LC to modify HF-MSCs.

PD-L1 Promotes Myofibroblastic Activation of Hepatic Stellate Cells by Distinct Mechanisms Selective for TGF-β Receptor I versus II

[Cell Reports] To determine the role of programmed death-ligand 1 (PD-L1) in myofibroblastic activation of hepatic stellate cells (HSCs), researchers disrupted PD-L1 of HSCs by shRNA or anti-PD-L1 antibody.

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