Results 171 to 180 of about 188,535 (344)
Prevalence of and risk factors for non-alcoholic fatty liver disease (NAFLD) in community-dwellers of Beijing, China [PDF]
G Li +5 more
openalex +1 more source
THE ROLE OF HYPERURICEMIA IN THE DEVELOPMENT OF NON-ALCOHOLIC FATTY LIVER DISEASE
М. Е. Стаценко +5 more
openalex +1 more source
Association of TNF-α, IGF-1, and IGFBP-1 levels with the severity of osteopenia in mice with non-alcoholic fatty liver disease [PDF]
Tong-Hao Wang +5 more
openalex +1 more source
Endothelial dysfunction in adolescents and young adults with nonalcoholic liver disease [PDF]
Nonalcoholic liver disease is a global public health problem that increases cardiovascular morbidity and mortality in these patients. This paper discusses endothelial dysfunction among patients (adolescents and young adults) with nonalcoholic liver ...
Donoiu, Ionuț +6 more
core +1 more source
RIPK3 Orchestrates Scar‐Associated Macrophage Dysfunction to Drive Pulmonary Fibrosis
Beyond signaling cell death, RIPK3 emerges as a critical metabolic regulator in pulmonary fibrosis. This research reveals that RIPK3 promotes PI3K‐AKT signaling in scar‐associated macrophages to fuel polyamine synthesis, independent of its kinase activity.
Tao Yang +12 more
wiley +1 more source
Diabetes is an independent risk factor for gallstones. It upregulates CXCR2 expression in hepatic neutrophils, stimulating the formation of NETs that disrupt hepatocellular tight junctions and the liver‐bile barrier. NETs enter bile to accelerate gallstone development, while sarcosine inhibits CXCR2 and NETs production, effectively reducing diabetes ...
Chao Shi +10 more
wiley +1 more source
Association of circulating preptin with non-alcoholic fatty liver disease: A case-control study
Derya Arğun +3 more
openalex +2 more sources
Red Blood Cell-Conditioned Media from Non-Alcoholic Fatty Liver Disease Patients Contain Increased MCP1 and Induce TNF-α Release [PDF]
Charalampos Papadopoulos +5 more
openalex +1 more source
Our study identifies selenium deficiency as a hallmark of MASH pathogenesis. Dietary selenium supplementation enhances hepatic fatty acid oxidation (FAO) and attenuates MASH progression by activating the PPARα pathway via selenoprotein H (SELENOH). This selenium‐SELENOH‐PPARα nexus redefines the functional scope of selenoproteins, moving from redox ...
Yuwei Zhang +11 more
wiley +1 more source

