eprintid: 118 rev_number: 12 eprint_status: archive userid: 2 importid: 0 dir: disk0/00/00/01/18 datestamp: 2021-05-31 14:17:26 lastmod: 2023-07-03 23:30:16 status_changed: 2021-05-31 14:17:26 type: article succeeds: 0 commentary: 0 metadata_visibility: show item_issues_count: 0 sword_depositor: 0 creators_name: Gallego, Paloma creators_name: Castejón-Vega, Beatriz creators_name: del Campo, José A. creators_name: Cordero, Mario D. creators_id: creators_id: creators_id: creators_id: mario.cordero@uneatlantico.es title: The Absence of NLRP3-inflammasome Modulates Hepatic Fibrosis Progression, Lipid Metabolism, and Inflammation in KO NLRP3 Mice during Aging ispublished: pub subjects: uneat_bm divisions: uneatlantico_produccion_cientifica full_text_status: none keywords: NLRP3-inflammasome complex; Inflammation; Liver damage; Non-alcoholic fatty liver disease; Oxidative stress. abstract: Aging 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. date: 2020-09 date_type: published publication: Cells volume: 9 number: 10 pagerange: 2148 pages: 0 id_number: doi:10.3390/cells9102148 refereed: TRUE issn: 2073-4409 official_url: http://doi.org/10.3390/cells9102148 num_pieces: 0 gscholar_impact: 0 gscholar_datestamp: 0000-00-00 00:00:00 access: open language: en citation: Artículo Materias > Biomedicina Universidad Europea del Atlántico > Investigación > Producción Científica Abierto Inglés Aging 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. metadata Gallego, Paloma; Castejón-Vega, Beatriz; del Campo, José A. y Cordero, Mario D. mail SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, mario.cordero@uneatlantico.es (2020) The Absence of NLRP3-inflammasome Modulates Hepatic Fibrosis Progression, Lipid Metabolism, and Inflammation in KO NLRP3 Mice during Aging. Cells, 9 (10). p. 2148. ISSN 2073-4409