{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["28(9)"],"submitter":["Kojima R"],"funding":["Mitsubishi Foundation","Japan Foundation of Applied Enzymology","Public Interest Incorporated Foundation Lotte Foundation","The Takeda Foundation","Sapporo Bioscience Foundation","Uehara Memorial Foundation","Government of Japan Ministry of Health Labour and Welfare","Japan Foundation for Aging and Health","Japan Society for the Promotion of Science"],"pubmed_abstract":["<i>trans-</i>Fatty acids (TFAs) have been associated with various inflammatory diseases, including atherosclerosis and metabolic syndrome, such as metabolic dysfunction-associated steatotic liver disease (MASLD)/metabolic dysfunction-associated steatohepatitis (MASH). However, the underlying mechanism remains unclear. Here, we show that in response to DNA damage, elaidic acid (EA), a most common TFA, amplifies interleukin-1 receptor (IL-1R) signaling, leading to the promotion of cellular senescence and senescence-associated secretory phenotype (SASP). Upon DNA damage, EA enhanced senescence-associated β-galactosidase activity and expressions of IL-1α/6/8 through the IL-1R-transforming growth factor-β-activated kinase 1 (TAK1)-nuclear factor (NF)-κB axis in a manner dependent on mammalian t"],"journal":["iScience"],"pagination":["113305"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12396248"],"repository":["biostudies-literature"],"pubmed_title":["Elaidic acid drives cellular senescence and inflammation via lipid raft-mediated IL-1R signaling."],"pmcid":["PMC12396248"],"pubmed_authors":["Noguchi T","Kojima R","Sato E","Ashida R","Matsuzawa A","Yokoyama K","Watanabe A","Matsui R","Hirata Y","Takita R","Abe T","Takahashi M","Hama K"],"additional_accession":[]},"is_claimable":false,"name":"Elaidic acid drives cellular senescence and inflammation via lipid raft-mediated IL-1R signaling.","description":"<i>trans-</i>Fatty acids (TFAs) have been associated with various inflammatory diseases, including atherosclerosis and metabolic syndrome, such as metabolic dysfunction-associated steatotic liver disease (MASLD)/metabolic dysfunction-associated steatohepatitis (MASH). However, the underlying mechanism remains unclear. Here, we show that in response to DNA damage, elaidic acid (EA), a most common TFA, amplifies interleukin-1 receptor (IL-1R) signaling, leading to the promotion of cellular senescence and senescence-associated secretory phenotype (SASP). Upon DNA damage, EA enhanced senescence-associated β-galactosidase activity and expressions of IL-1α/6/8 through the IL-1R-transforming growth factor-β-activated kinase 1 (TAK1)-nuclear factor (NF)-κB axis in a manner dependent on mammalian t","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-05-29T17:19:38.079Z","creation":"2026-04-08T05:29:33.099Z"},"accession":"S-EPMC12396248","cross_references":{"pubmed":["40894877"],"doi":["10.1016/j.isci.2025.113305"]}}