Results 121 to 130 of about 210,456 (335)

CHB‐Induced Immune Zonation Chaos Elicited LXRα‐mediated Lipid Metabolism Disorders in Kupffer Cells to Induce Cancer Stem Cell Formation

open access: yesAdvanced Science, EarlyView.
By profiling the spatiotemporal hepatic landscape of CHB mouse models, the originally peri‐portal localized KCs migrated to the peri‐central in a CXCL9‐CXCR3‐dependent manner, facilitating their interaction with HBV+ hepatocytes. The interaction promoted LMD in KCs through ASGR1‐induced LXRα degradation, which, in turn, induced CSC formation via Stat3 ...
Jingqi Shi   +18 more
wiley   +1 more source

New insights into the pathogenesis and treatment of non-viral hepatocellular carcinoma: a balancing act between immunosuppression and immunosurveillance. [PDF]

open access: yes, 2018
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. HCC initiates as a consequence of chronic liver damage and inflammation caused by hepatitis B and C virus infections, excessive alcohol consumption, or non ...
Karin, Michael
core   +1 more source

Transforming Growth Factor Beta-Induced Foxo3a Acts as a Profibrotic Mediator in Hepatic Stellate Cells [PDF]

open access: bronze, 2020
Seung Jung Kim   +9 more
openalex   +1 more source

The role of the apoptosis-related protein BCL-B in the regulation of mitophagy in hepatic stellate cells during the regression of liver fibrosis

open access: yesExperimental and Molecular Medicine, 2019
The clearance of activated hepatic stellate cells (HSCs) by apoptosis is critical for the reversibility of hepatic fibrosis. Mitochondrial homeostasis is regulated by mitophagy, which is an efficient way of clearing injured mitochondria that plays an ...
Qian Ding   +10 more
semanticscholar   +1 more source

PARPi Combining Nanoparticle LIN28B siRNA for the Management of Malignant Ascites

open access: yesAdvanced Science, EarlyView.
This study demonstrates that co‐inhibition of LIN28B and PARP using siLin28b/DSSP@lip‐PEG‐FA nanoparticles in combination with the PARP inhibitor BMN673 effectively suppresses the accumulation of malignant ascites associated with advanced cancers.
Yan Fang   +13 more
wiley   +1 more source

Expression patterns of STAT3, ERK and estrogen-receptor α are associated with development and histologic severity of hepatic steatosis: a retrospective study

open access: yesDiagnostic Pathology, 2018
Background Hepatic steatosis renders hepatocytes vulnerable to injury, resulting in the progression of preexisting liver disease. Previous animal and cell culture studies implicated mammalian target of rapamycin (mTOR), signal transducer and activator of
Euno Choi   +7 more
doaj   +1 more source

Cancer-Associated Thrombosis in Cirrhotic Patients with Hepatocellular Carcinoma. [PDF]

open access: yes, 2018
It is common knowledge that cancer patients are more prone to develop venous thromboembolic complications (VTE). It is therefore not surprising that patients with hepatocellular carcinoma (HCC) present with a significant risk of VTE, with the portal vein
Burra, P   +5 more
core   +1 more source

Hepatic stellate cells maintain liver homeostasis through paracrine neurotrophin-3 signaling

open access: yesbioRxiv, 2023
V. Q. Trinh   +11 more
semanticscholar   +1 more source

Exosomes derived from palmitic acid-treated hepatocytes induce fibrotic activation of hepatic stellate cells

open access: yesScientific Reports, 2017
Non-alcoholic fatty liver disease (NAFLD) is a dominant cause of chronic liver disease, but the exact mechanism of progression from simple steatosis to nonalcoholic steatohepatitis (NASH) remains unknown.
Young-Sun Lee   +15 more
semanticscholar   +1 more source

p16Ink4a‐Positive Hepatocytes Drive Liver Fibrosis Through Activation of LIFR Family Pathway

open access: yesAdvanced Science, EarlyView.
This study found that, following the long‐term CCl4 treatment, p16high hepatocytes appeared in zone 3, spatially co‐localizing with fibrotic areas. A specific cluster of p16high hepatocytes upregulated CTF1/LIF expression which induced HSC activation and further liver fibrosis, as revealed by single cell transcriptomic analysis.
Koji Nishikawa   +23 more
wiley   +1 more source

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