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Altered mitochondrial unfolded protein response and FGF21 secretion in MASLD progression and the effect of exercise intervention.
Sci Rep
January 2025
School of Sports and Health, Nanjing Sport Institute, Nanjing, China.
A high-calorie diet and lack of exercise are the most important risk factors contributing to metabolic dysfunction-associated steatotic liver disease (MASLD) initiation and progression. The precise molecular mechanisms of mitochondrial function alteration during MASLD development remain to be fully elucidated. In this study, a total of 60 male C57BL/6J mice were maintained on a normal or amylin liver NASH (AMLN) diet for 6 or 10 weeks.
View Article and Find Full Text PDF"Evaluation of Curcuma zedoaria Rosc. in the management of non-alcoholic fatty liver Disease: A Randomized, single blind, controlled trial".
Arab J Gastroenterol
January 2025
PG Dept. of Moalajat, (Medicine) RRIUM, Srinagar, India.
Background And Study Aims: Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disorder, affecting 23% to 32% of the global population. This clinical study aimed to assess the efficacy of Curcuma zedoaria Rosc. compared to vitamin E in managing NAFLD.
View Article and Find Full Text PDFThe PPAR-α agonist oleoyethanolamide (OEA) ameliorates valproic acid-induced steatohepatitis in rats via suppressing Wnt3a/β-catenin and activating PGC-1α: Involvement of network pharmacology and molecular docking.
Eur J Pharmacol
January 2025
Pharmacology & Environmental Toxicology, Environmental Studies & Research Institute (ESRI), University of Sadat City, Sadat City 32897, Menoufia, Egypt. Electronic address:
Liver damage is one of the most severe side effects of valproic acid (VPA) therapy. Research indicates that PPAR-α prevents Wnt3a/β-catenin-induced PGC-1α dysregulation, which is linked to liver injury. Although PPAR-α activation has hepatoprotective effects, its role in preventing VPA-induced liver injury remains unclear.
View Article and Find Full Text PDFNon-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic liver disorder worldwide, and effective therapeutic strategies for its treatment remains limited. In this article, we introduced Glipo-siRubi, a hepatocytes-targeting RNA interference (RNAi) nanoliposome for suppression of Rubicon expression, aiming to achieve precise regulation of autophagy in NAFLD. Autophagy activation induced by Rubicon suppression resulted in reduced endoplasmic reticulum stress and intracellular lipid accumulation in vitro.
View Article and Find Full Text PDFBackground And Aim: There is paucity of data about the prevalence of cirrhosis and portal hypertension in the US general population.
Methods: We used National Health and Nutrition Examination Surveys (NHANES 2017-2020) to estimate the prevalence of cirrhosis and clinically significant (CS)-portal hypertension in alcoholic liver disease (ALD), MetALD, viral hepatitis (VH) to include chronic hepatitis B (CHB) and chronic hepatitis C (CHC), and metabolic dysfunction-associated steatotic liver disease (MASLD). Cirrhosis was evaluated using liver stiffness measurement (LSM) by transient elastography or FIB-4 score; CS-portal hypertension was defined via LSM and platelet count or the use of non-selective beta-blockers in the presence of cirrhosis.
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