Gallego, PalomaCastejón-Vega, BeatrizDel Campo, José ACordero, Mario D2023-02-092023-02-092020-09-23http://hdl.handle.net/10668/16318Aging is associated with metabolic changes and low-grade inflammation in several organs, which may be due to NLRP3 inflammasome activation. Methods: Here, we asked whether age-related liver changes such as lipid metabolism and fibrosis are reduced in aged mice lacking the NLRP3 inflammasome. We report reduced protein levels of lipid markers (MTP, FASN, DGAT1), SOD activity, oxidative stress marker PTPRG, and the fibrotic markers TPM2β, COL1-α1 associated with increased GATA4, in NLRP3 deficient mice. Fibrotic, lipid, and oxidative reduction in liver tissues of mice was more pronounced in those old KO NLRP3 mice than in the younger ones, despite their greater liver damage. These results suggest that absence of the NLRP3 inflammasome attenuates age-related liver fibrotic pathology in mice, suggesting that pharmacological targeting may be beneficial.enAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/NLRP3-inflammasome complexinflammationliver damagenon-alcoholic fatty liver diseaseoxidative stressAnimalsBiomarkersCarrier ProteinsInflammasomesInflammationLipid MetabolismLiver CirrhosisMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinThe Absence of NLRP3-inflammasome Modulates Hepatic Fibrosis Progression, Lipid Metabolism, and Inflammation in KO NLRP3 Mice during Aging.research article32977490open access10.3390/cells91021482073-4409PMC7598267https://www.mdpi.com/2073-4409/9/10/2148/pdf?version=1601208407https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7598267/pdf