ArticlePloS one2017
Microvesicles released from fat-laden cells promote activation of hepatocellular NLRP3 inflammasome: A pro-inflammatory link between lipotoxicity and non-alcoholic steatohepatitis.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 62 citations in OpenAlex.
- Emricasan (IDN-6556) Lowers Portal Pressure in Patients With Compensated Cirrhosis and Severe Portal Hypertension.Hepatology (Baltimore, Md.) · 2019Trial
- The Role of the OSM/OSMRβ Axis in Chronic Liver Disease Progression and Hepatocellular Carcinoma Development: A Focus on MASLD/MASH.International journal of molecular sciences · 2026Review
- Free Fatty Acids Correlate with the Interleukin-1 β and Interleukin-1 Receptor Antagonist in the Early Subacute Phase of Stroke.Biomolecules · 2025Article
- Extracellular vesicles for targeted drug delivery: advances in surface modification strategies and therapeutic applications.Journal of translational medicine · 2025Review
- The role of extracellular vesicles in non-alcoholic steatohepatitis: Emerging mechanisms, potential therapeutics and biomarkers.Journal of advanced research · 2025Review
- NLRP3 inflammasome inhibition decreasesInfection and immunity · 2024Article
- MASLD-Related Hepatocarcinoma: Special Features and Challenges.Journal of clinical medicine · 2024Review
- Exosomes: Nomenclature, Isolation, and Biological Roles in Liver Diseases.Biomolecules & therapeutics · 2023Review
- Periodontitis, chronic liver diseases, and the emerging oral-gut-liver axis.Periodontology 2000 · 2022Review
- Cell-to-Cell Communications in Alcohol-Associated Liver Disease.Frontiers in physiology · 2022Article
- Nonalcoholic Fatty Liver Disease (NAFLD): Pathogenesis and Noninvasive Diagnosis.Biomedicines · 2021Review
- Review
- Extracellular Vesicles as Drivers of Non-Alcoholic Fatty Liver Disease: Small Particles with Big Impact.Biomedicines · 2021Review
- Extracellular Vesicles in the Development of the Non-Alcoholic Fatty Liver Disease: An Update.Biomolecules · 2020Review
- Article
- Complement Properdin Regulates the Metabolo-Inflammatory Response to a High Fat Diet.Medicina (Kaunas, Lithuania) · 2020Article
- Review
- Adaptive immunity: an emerging player in the progression of NAFLD.Nature reviews. Gastroenterology & hepatology · 2020Review
- Extracellular Vesicles as Inflammatory Drivers in NAFLD.Frontiers in immunology · 2020Review
- Nonalcoholic fatty liver disease and portal hypertension.Exploration of medicine · 2020Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-Alcoholic Fatty Liver Disease (NAFLD) is a major form of chronic liver disease in the general population in relation to its high prevalence among overweight/obese individuals and patients with diabetes type II or metabolic syndrome. NAFLD can progress to steatohepatitis (NASH), fibrosis and cirrhosis and end-stage of liver disease but mechanisms involved are still incompletely characterized. Within the mechanisms proposed to mediate the progression of NAFLD, lipotoxicity is believed to play a major role. In the present study we provide data suggesting that microvesicles (MVs) released by fat-laden cells undergoing lipotoxicity can activate NLRP3 inflammasome following internalization by either cells of hepatocellular origin or macrophages. Inflammasome activation involves NF-kB-mediated up-regulation of NLRP3, pro-caspase-1 and pro-Interleukin-1, then inflammasome complex formation and Caspase-1 activation leading finally to an increased release of IL-1β. Since the release of MVs from lipotoxic cells and the activation of NLRP3 inflammasome have been reported to occur in vivo in either clinical or experimental NASH, these data suggest a novel rational link between lipotoxicity and increased inflammatory response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.