{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["43(3)"],"submitter":["Mirea AM"],"funding":["Else Kröner-Fresenius-Stiftung"],"pubmed_abstract":["Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. Inflammatory pathways contribute to disease pathogenesis; however, regulation of the underlying mechanism is not completely understood. IL-1β, a pro-inflammatory cytokine, participates in the development and progression of NAFLD. To become bioactive, IL-1β requires enzymatic processing. Mechanisms that activate IL-1β include the classical NLRP3 inflammasome-caspase-1 and the neutrophil serine proteases, neutrophil elastase, and proteinase-3. Several studies have shown that both caspase-1 and the neutrophil serine proteases are important for NAFLD development. However, it is unknown whether these pathways interact and if they have a synergistic effect in promoting NAFLD. In the present study, we dev"],"journal":["Inflammation"],"pagination":["1054-1064"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7280336"],"repository":["biostudies-literature"],"pubmed_title":["Mice Deficient in the IL-1β Activation Genes Prtn3, Elane, and Casp1 Are Protected Against the Development of Obesity-Induced NAFLD."],"pmcid":["PMC7280336"],"pubmed_authors":["Chavakis T","Joosten LAB","Kanneganti TD","Mirea AM","Tack CJ","Toonen EJM","Stienstra R"],"additional_accession":[]},"is_claimable":false,"name":"Mice Deficient in the IL-1β Activation Genes Prtn3, Elane, and Casp1 Are Protected Against the Development of Obesity-Induced NAFLD.","description":"Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. Inflammatory pathways contribute to disease pathogenesis; however, regulation of the underlying mechanism is not completely understood. IL-1β, a pro-inflammatory cytokine, participates in the development and progression of NAFLD. To become bioactive, IL-1β requires enzymatic processing. Mechanisms that activate IL-1β include the classical NLRP3 inflammasome-caspase-1 and the neutrophil serine proteases, neutrophil elastase, and proteinase-3. Several studies have shown that both caspase-1 and the neutrophil serine proteases are important for NAFLD development. However, it is unknown whether these pathways interact and if they have a synergistic effect in promoting NAFLD. In the present study, we dev","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Jun","modification":"2025-04-22T18:29:39.754Z","creation":"2020-06-20T07:07:39Z"},"accession":"S-EPMC7280336","cross_references":{"pubmed":["32002713"],"doi":["10.1007/s10753-020-01190-4"]}}