biostudies-literatureUnknown28(9)Kojima RMitsubishi FoundationJapan Foundation of Applied EnzymologyPublic Interest Incorporated Foundation Lotte FoundationThe Takeda FoundationSapporo Bioscience FoundationUehara Memorial FoundationGovernment of Japan Ministry of Health Labour and WelfareJapan Foundation for Aging and HealthJapan Society for the Promotion of Science<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 tiScience113305https://www.ebi.ac.uk/biostudies/studies/S-EPMC12396248biostudies-literatureElaidic acid drives cellular senescence and inflammation via lipid raft-mediated IL-1R signaling.PMC12396248Noguchi TKojima RSato EAshida RMatsuzawa AYokoyama KWatanabe AMatsui RHirata YTakita RAbe TTakahashi MHama KfalseElaidic acid drives cellular senescence and inflammation via lipid raft-mediated IL-1R signaling.<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 t2025-01-01T00:00:00Z2025 Sep2026-05-29T17:19:38.079Z2026-04-08T05:29:33.099ZS-EPMC123962484089487710.1016/j.isci.2025.113305