<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>43(3)</volume><submitter>Mirea AM</submitter><funding>Else Kröner-Fresenius-Stiftung</funding><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</pubmed_abstract><journal>Inflammation</journal><pagination>1054-1064</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7280336</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Mice Deficient in the IL-1β Activation Genes Prtn3, Elane, and Casp1 Are Protected Against the Development of Obesity-Induced NAFLD.</pubmed_title><pmcid>PMC7280336</pmcid><pubmed_authors>Chavakis T</pubmed_authors><pubmed_authors>Joosten LAB</pubmed_authors><pubmed_authors>Kanneganti TD</pubmed_authors><pubmed_authors>Mirea AM</pubmed_authors><pubmed_authors>Tack CJ</pubmed_authors><pubmed_authors>Toonen EJM</pubmed_authors><pubmed_authors>Stienstra R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mice Deficient in the IL-1β Activation Genes Prtn3, Elane, and Casp1 Are Protected Against the Development of Obesity-Induced NAFLD.</name><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</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jun</publication><modification>2025-04-22T18:29:39.754Z</modification><creation>2020-06-20T07:07:39Z</creation></dates><accession>S-EPMC7280336</accession><cross_references><pubmed>32002713</pubmed><doi>10.1007/s10753-020-01190-4</doi></cross_references></HashMap>