ArticleAnimal models and experimental medicine2024
Perilipin 5 regulates hepatic stellate cell activation and high-fat diet-induced non-alcoholic fatty liver disease.
Article in Animal models and experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 14 citations in OpenAlex.
- Psoralidin, a main compound in Psoraleae Fructus, induces hepatotoxicity by impeding lipid oxidative catabolism and aggravating lipid accumulation in mice.Chinese medicine · 2026Article
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- The role of mitochondrial DNA and RNA in promoting liver disease pathogenesis.Frontiers in cell and developmental biology · 2026Review
- Exercise and cold exposure as dual physiological stressors in MASLD: AMPK-mediated metabolic adaptation and interorgan crosstalk.Frontiers in physiology · 2026Review
- Exercise attenuates hepatic ectopic lipid deposition in high fat-diet rats via PKA-mediated phosphorylation of Perilipin5.Scientific reports · 2025Article
- Interactions between lipid droplets and mitochondria in metabolic diseases.Lipids in health and disease · 2025Review
- Article
- Metabolic Sparks in the Liver: Metabolic and Epigenetic Reprogramming in Hepatic Stellate Cells Activation and Its Implications for Human Metabolic Diseases.Diabetes & metabolism journal · 2025Review
- Alterations in Glutathione Redox Homeostasis in Metabolic Dysfunction-Associated Fatty Liver Disease: A Systematic Review.Antioxidants (Basel, Switzerland) · 2024Review
- Perilipin 5 regulates hepatic stellate cell activation and high-fat diet-induced non-alcoholic fatty liver disease.Animal models and experimental medicine · 2024Article
- Perilipin 5 deletion protects against nonalcoholic fatty liver disease and hepatocellular carcinoma by modulating lipid metabolism and inflammatory responses.Cell death discovery · 2024Article
- Inter-organ metabolic interaction networks in non-alcoholic fatty liver disease.Frontiers in endocrinology · 2024Review
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13 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundNonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases globally. Hepatic stellate cells (HSCs) are the major effector cells of liver fibrosis. HSCs contain abundant lipid droplets (LDs) in their cytoplasm during quiescence. Perilipin 5 (PLIN 5) is a LD surface-associated protein that plays a crucial role in lipid homeostasis. However, little is known about the role of PLIN 5 in HSC activation.
methodsPLIN 5 was overexpressed in HSCs of Sprague-Dawley rats by lentivirus transfection. At the same time, PLIN 5 gene knockout mice were constructed and fed with a high-fat diet (HFD) for 20 weeks to study the role of PLIN 5 in NAFLD. The corresponding reagent kits were used to measure TG, GSH, Caspase 3 activity, ATP level, and mitochondrial DNA copy number. Metabolomic analysis of mice liver tissue metabolism was performed based on UPLC-MS/MS. AMPK, mitochondrial function, cell proliferation, and apoptosis-related genes and proteins were detected by western blotting and qPCR.
resultsOverexpression of PLIN 5 in activated HSCs led to a decrease in ATP levels in mitochondria, inhibition of cell proliferation, and a significant increase in cell apoptosis through AMPK activation. In addition, compared with the HFD-fed C57BL/6J mice, PLIN 5 knockout mice fed with HFD showed reduced liver fat deposition, decreased LD abundance and size, and reduced liver fibrosis.
conclusionThese findings highlight the unique regulatory role of PLIN 5 in HSCs and the role of PLIN 5 in the fibrosis process of NAFLD.
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