Autophagy is a highly conserved intracellular catabolic pathway that degrades cellular long-lived proteins and organelles. Autophagy is normally activated in response to nutrient deprivation and other stresses as a cell survival mechanism. Accumulating evidence indicates that autophagy plays a critical role in liver pathophysiology, in addition to maintaining hepatic energy and nutrient balance. Alcohol consumption causes hepatic metabolic changes, oxidative stress, accumulation of lipid droplets and damaged mitochondria; all of these can be regulated by autophagy. This review summarizes the recent findings about the role and mechanisms of autophagy in alcoholic liver disease (ALD), and the possible intervention for treating ALD by modulating autophagy.
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http://dx.doi.org/10.1258/ebm.2011.010360 | DOI Listing |
Medicina (Kaunas)
January 2025
Department of Anatomy and Physiology, College of Medicine, Imam Mohammad Ibn Saud Islamic University (IMSIU), Riyadh 13317, Saudi Arabia.
: High fructose intake is associated with non-alcoholic fatty liver disease (NAFLD), a chronic liver disease that is on the rise worldwide. New alternatives for treatment, such as bioactive phytochemicals, are needed. The aim of this study was to investigate the beneficial role of resveratrol in treating non-alcoholic steatohepatitis (NASH).
View Article and Find Full Text PDFComput Struct Biotechnol J
December 2024
National Vaccine Innovation Platform, Scholl of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Unlabelled: The prevention and treatment of metabolic disorders, such as non-alcoholic fatty liver disease (NAFLD), have emerged as critical global health challenges. Current lipid-lowering pharmacotherapies are associated with side effects, including hepatotoxicity, rhabdomyolysis, and decreased erythrocyte counts, underscoring the urgent need for safer therapeutic alternatives. Hepatocyte nuclear factor 4α (HNF4α) has been identified as a pivotal regulator of lipid metabolism, making it an attractive target for drug development.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
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 PDFFront Microbiol
January 2025
Department of Infectious Disease, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Objective: This study investigates the protective effects of lactic acid, a metabolite of , on non-alcoholic fatty liver disease (NAFLD) induced by a high-sugar, high-fat diet (HFD) in mice, in the context of the gut-liver axis.
Methods: A NAFLD mouse model was established using a HFD, and different intervention groups were set up to study the protective effects of and its metabolite lactic acid. The groups included a control group, NAFLD group, treatment group, Glyceraldehyde-3-P (G-3P) co-treatment group, and NOD-like receptor family pyrin domain containing 3 (NLRP3) overexpression group.
Front Pharmacol
January 2025
Department of Clinical Pharmacy, Meizhou People's Hospital (Huangtang Hospital), Meizhou, China.
Objective: Non-alcoholic steatohepatitis (NASH) is a progressive liver disease with lipid accumulation, inflammation, and liver fibrosis. Ponatinib, a third-generation tyrosine kinase inhibitors for the treatment of chronic myeloid leukemia, was found to improve metabolic disorders in mice. However, the role of ponatinib in liver inflammation and fibrosis remains to be elucidated.
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