Results 11 to 20 of about 79,018 (355)

Hepatic Stellate Cells and Hepatocarcinogenesis [PDF]

open access: yesFrontiers in Cell and Developmental Biology, 2020
Hepatic stellate cells (HSCs) are a significant component of the hepatocellular carcinoma (HCC) tumor microenvironment (TME). Activated HSCs transform into myofibroblast-like cells to promote fibrosis in response to liver injury or chronic inflammation ...
Anna E. Barry   +12 more
doaj   +3 more sources

Hepatic stellate cell progenitor cells [PDF]

open access: yesJournal of Gastroenterology and Hepatology, 2012
AbstractHepatic stellate cells (HSCs) are recognized as a major player in liver fibrogenesis. Upon liver injury, HSCs differentiate into myofibroblasts and participate in progression of fibrosis and cirrhosis. Additional cell types such as resident liver fibroblasts/myofibroblasts or bone marrow cells are also known to generate myofibroblasts.
openaire   +2 more sources

Co-targeting HGF/cMET Signaling with MEK Inhibitors in Metastatic Uveal Melanoma. [PDF]

open access: yes, 2017
Patients with metastatic uveal melanoma usually die within 1 year of diagnosis, emphasizing an urgent need to develop new treatment strategies. The liver is the most common site of metastasis.
Aplin, Andrew E.   +8 more
core   +2 more sources

Hepatic Stellate Cells Support Hematopoiesis and are Liver-Resident Mesenchymal Stem Cells

open access: yesCellular Physiology and Biochemistry, 2013
Background/Aims: Hematopoiesis can occur in the liver, when the bone marrow fails to provide an adequate environment for hematopoietic stem cells.
Claus Kordes   +3 more
doaj   +1 more source

The C-type lectin COLEC10 is predominantly produced by hepatic stellate cells and involved in the pathogenesis of liver fibrosis

open access: yesCell Death and Disease, 2023
Hepatic stellate cell is one of the major nonparenchymal cell types in liver. It has been proved the hepatic stellate cells are activated upon liver injury and produce excessive extracellular matrix to induce liver fibrosis.
Mengfan Zhang   +9 more
doaj   +1 more source

SerpinB3 promotes pro-fibrogenic responses in activated hepatic stellate cells [PDF]

open access: yes, 2017
SerpinB3 is a hypoxia- and hypoxia-inducible factor-2\u3b1-dependent cystein protease inhibitor that is up-regulated in hepatocellular carcinoma and in parenchymal cells during chronic liver diseases (CLD). SerpinB3 up-regulation in CLD patients has been
Albano, Emanuele   +16 more
core   +3 more sources

Extracellular Vesicles from Steatotic Hepatocytes Provoke Pro-Fibrotic Responses in Cultured Stellate Cells

open access: yesBiomolecules, 2022
Hepatic steatosis and chronic hepatocyte damage ultimately lead to liver fibrosis. Key pathophysiological steps are the activation and transdifferentiation of hepatic stellate cells.
Maria Teresa Koenen   +10 more
doaj   +1 more source

Role of cytoglobin, a novel radical scavenger, in stellate cell activation and hepatic fibrosis [PDF]

open access: yesClinical and Molecular Hepatology, 2020
Cytoglobin (Cygb), a stellate cell-specific globin, has recently drawn attention due to its association with liver fibrosis. In the livers of both humans and rodents, Cygb is expressed only in stellate cells and can be utilized as a marker to distinguish
Le Thi Thanh Thuy   +2 more
doaj   +1 more source

Different effects of rat interferon alpha, beta and gamma on rat hepatic stellate cell proliferation and activation

open access: yesBMC Cell Biology, 2002
Background Liver fibrosis is the common sequel of chronic liver diseases. Recent studies have identified hepatic stellate cells as the primary cell type mediating hepatic fibrogenesis.
Minuk Gerald Y   +3 more
doaj   +1 more source

A Selective PPARγ Modulator Reduces Hepatic Fibrosis

open access: yesBiology, 2020
Hepatic fibrosis is the accumulation of excess collagen as a result of chronic liver injury. If left unabated, hepatic fibrosis can lead to the disruption of the liver architecture, portal hypertension, and increased risk of progression to cirrhosis and ...
Benita L. McVicker   +3 more
doaj   +1 more source

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