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| http://dx.doi.org/10.21037/hbsn-23-196 | DOI Listing |
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Progressive systemic inflammation precedes decompensation in compensated cirrhosis.
JHEP Rep
February 2025
Department of Gastroenterology and Hepatology, Hospital Universitario Ramón y Cajal, Instituto Ramon y Cajal de Investigación Sanitaria (IRYCIS), Universidad de Alcalá, Madrid, Spain.
Background & Aims: Systemic inflammation is a driver of decompensation in cirrhosis with unclear relevance in the compensated stage. We evaluated inflammation and bacterial translocation markers in compensated cirrhosis and their dynamics in relation to the first decompensation.
Methods: This study is nested within the PREDESCI trial, which investigated non-selective beta-blockers for preventing decompensation in compensated cirrhosis and clinically significant portal hypertension (CSPH: hepatic venous pressure gradient ≥10 mmHg).
Inter-organ metabolic interaction networks in non-alcoholic fatty liver disease.
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State Key Laboratory of New Targets Discovery and Drug Development for Major Diseases, Gannan Innovation and Translational Medicine Research Institute, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, Gannan Medical University, Ganzhou, China.
Non-alcoholic fatty liver disease (NAFLD) is a multisystem metabolic disorder, marked by abnormal lipid accumulation and intricate inter-organ interactions, which contribute to systemic metabolic imbalances. NAFLD may progress through several stages, including simple steatosis (NAFL), non-alcoholic steatohepatitis (NASH), cirrhosis, and potentially liver cancer. This disease is closely associated with metabolic disorders driven by overnutrition, with key pathological processes including lipid dysregulation, impaired lipid autophagy, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and local inflammation.
View Article and Find Full Text PDFMetabolic dysfunction-associated steatotic liver disease in children.
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Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of California San Diego School of Medicine, La Jolla, California, USA
Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease, is the most common cause of chronic liver disease in children. MASLD encompasses a spectrum of liver disease and can be severe, with 10% of affected children presenting with advanced fibrosis. While biopsy remains the most accurate method for diagnosing and staging the disease, MRI proton density fat fraction and magnetic resonance elastography are the most reliable non-invasive measures for assessing steatosis and fibrosis, respectively.
View Article and Find Full Text PDFAescin ameliorates alcohol-induced liver injury. A possible implication of ROS / TNF-alpha / p38MAPK / caspase-3 signalling.
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Alcoholic liver disease (ALD) is a commonly known liver disease mediated by prolonged alcohol consumption. Aescin is a triterpene saponin that can manage several conditions, including brain trauma, arthritis, venous congestion, stroke, and thrombophlebitis. Even so, studies illustrating the aescin role in ALD are scarce.
View Article and Find Full Text PDFTitanium dioxide-induced fibrotic liver model and the therapeutic effect of resveratrol by modulation of α-SMA and 8-oHdG expressions, oxidative stress, and inflammation.
Tissue Cell
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Karabuk University, Faculty of Medicine, Department of Medical Biochemistry, Karabuk, Turkey.
The research sought to assess the therapeutic impact of resveratrol by biochemical, immunohistochemical, and histopathological analyses in a TiO-induced liver fibrosis model. Titanium dioxide (100 mg/kg body weight) was delivered for 15 days to induce liver fibrosis, either alone or in conjunction with resveratrol (30 mg/kg body weight) therapy for the same duration. Resveratrol has been identified as a crucial therapeutic drug that provides an alternative treatment method for TiO-induced liver fibrosis by mitigating inflammation, oxidative stress, and the expressions of α-SMA and 8-OHdG.
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