Results 51 to 60 of about 229,203 (309)
Liver stiffness promotes intrahepatic cholesterol accumulation by repressing LXRα through YAP/TAZ activation. Stiff matrices impair cholesterol efflux in hepatocytes, while YAP/TAZ deletion restores LXRα activity and prevents cholesterol‐induced fibrosis.
Na Young Lee +9 more
wiley +1 more source
Polycarbonate nanogels enable lipid‐free delivery of anti‐MFAP‐5 siRNA into cancer‐associated fibroblasts (CAF) in hepatocellular carcinoma. In a cirrhotic murine model, this approach silences MFAP‐5, reduces fibroblast activation, and suppresses tumor growth by inhibiting NOTCH/Hes1‐driven angiogenesis. CAF‐targeted MFAP‐5 RNAi and conserved signaling
Paul Schneider +20 more
wiley +1 more source
The regulatory role of IL-6R in hepatitis B-associated fibrosis and cirrhosis
This study investigated the expression and regulation of IL-6R in hepatitis B-associated moderate hepatic fibrosis and cirrhosis. Liver tissues, peripheral blood monocytes (PBMs) and serum were collected from 26 hepatitis B patients with liver fibrosis ...
Y. Chen, S. Yang, Y. Peng, Z. Yang
doaj +1 more source
Bile Acid Receptor Therapeutics Effects on Chronic Liver Diseases [PDF]
In the past ten years, our understanding of the importance of bile acids has expanded from fat absorption and glucose/lipid/energy homeostasis into potential therapeutic targets for amelioration of chronic cholestatic liver diseases.
Alpini, Gianfranco +4 more
core +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
Gut microbiota–derived short‐chain fatty acids regulate group 3 innate lymphoid cells in HCC
Abstract Background and Aims Type 3 innate lymphoid cells (ILC3s) are essential for host defense against infection and tissue homeostasis. However, their role in the development of HCC has not been adequately confirmed. In this study, we investigated the immunomodulatory role of short‐chain fatty acids (SCFAs) derived from intestinal microbiota in ILC3
Chupeng Hu +11 more
wiley +1 more source
Improved quality of life in patients with refractory or recidivant ascites after insertion of transjugular intrahepatic portosystemic shunts [PDF]
Background. We have recently shown that the transjugular intrahepatic portosystemic shunt (TIPS) is more effective than paracentesis in the treatment of cirrhotic patients with severe ascites and can prolong survival in selected patients.
Bilzer, M. +5 more
core +1 more source
Cleavage‐Resistant CYLD Protects Against Autoimmune Hepatitis
Proteolytic cleavage of the deubiquitinase CYLD emerges as a critical driver of autoimmune hepatitis. TNFα‐induced CYLD loss in macrophages amplifies S100A9‐triggered MAPK activation, leading to excessive chemokine production and hepatic inflammation. Pharmacological inhibition of MEK signaling effectively attenuates experimental disease, highlighting ...
Han Liu +13 more
wiley +1 more source
Abstract Background and Aims Peroxisome proliferator‐activated receptor α (PPARα) regulates fatty acid transport and catabolism in liver. However, the role of intestinal PPARα in lipid homeostasis is largely unknown. Here, intestinal PPARα was examined for its modulation of obesity and NASH. Approach and Results Intestinal PPARα was activated and fatty
Tingting Yan +22 more
wiley +1 more source
Role of the liver in splanchnic extraction of atrial natriuretic factor in the rat [PDF]
Mesenteric, hepatic and splanchnic extraction of C-terminal and N-terminal atrial natriuretic factor was investigated in male Sprague-Dawley rats. Plasma concentrations (mean ± S.E.M.) of C-terminal atrial natriuretic factor were 55.0 ± 6.1 fmol/ml, 31.2
Alexander L. Gerbes +39 more
core +1 more source

