Results 51 to 60 of about 125,716 (297)
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
Adaptive mitochondrial mechanisms allow mitochondrial resilience and prevent the worsening of fibrosis, while deregulation of these mechanisms promotes the progression from no/minimal‐mild (F0‐F2) fibrosis to advanced fibrosis and cirrhosis (F3‐F4). Abstract Background and Aims Hepatitis B virus (HBV) infection causes oxidative stress (OS) and alters ...
Dimitri Loureiro +17 more
wiley +1 more source
Background and Objectives: Non-alcoholic fatty liver disease (NAFLD) is highly prevalent worldwide. It progresses from simple steatosis to non-alcoholic steatohepatitis (NASH).
Carolina Guzmán +5 more
doaj +1 more source
Lipotoxic lethal and sublethal stress signaling in hepatocytes: relevance to NASH pathogenesis[S]
The accumulation of lipids is a histologic and biochemical hallmark of obesity-associated nonalcoholic fatty liver disease (NAFLD). A subset of NALFD patients develops progressive liver disease, termed nonalcoholic steatohepatitis, which is characterized
Petra Hirsova +3 more
doaj +1 more source
Nonalcoholic fatty liver disease, especially nonalcoholic steatohepatitis (NASH), has become a major cause of liver transplantation and liver‐associated death.
T. Lan +15 more
semanticscholar +1 more source
p16Ink4a‐Positive Hepatocytes Drive Liver Fibrosis Through Activation of LIFR Family Pathway
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
Janus kinase 2 inhibition by pacritinib as potential therapeutic target for liver fibrosis
Diagram of the activation of the profibrotic and procontractile Janus kinase 2 (JAK2)/Ras homolog family member A/Rho‐kinase pathway and the inhibition of phosphorylated JAK2 by pacritinib to inhibit hepatic stellate cell activity. Abstract Background and Aims Janus kinase 2 (JAK2) signaling is increased in human and experimental liver fibrosis with ...
Sandra Torres +21 more
wiley +1 more source
BACKGROUND & AIMS Nonalcoholic steatohepatitis (NASH) has been predicted to become the leading indication for liver transplantation (LT) in the United States.
R. Wong +6 more
semanticscholar +1 more source
An AMPK–caspase-6 axis controls liver damage in nonalcoholic steatohepatitis
Liver disease defect identified The energy sensor adenosine monophosphate–activated protein kinase (AMPK) is implicated in liver damage in nonalcoholic steatohepatitis (NASH), a leading cause of liver-associated death in humans. Zhao et al.
Peng Zhao +10 more
semanticscholar +1 more source
Normal bladders exhibit quiescent fibroblasts/macrophages, whereas neurogenic bladders show acute‐phase Itga8⁺ fibroblast expansion driven by Trem2⁺ macrophage‐secreted Fn1, which activates FAK/RhoA/ROCK signaling, promotes cytoskeletal remodeling, and upregulates pro‐fibrotic genes.
Jiaxin Wang +9 more
wiley +1 more source

