Matches in SemOpenAlex for { <https://semopenalex.org/work/W3049145469> ?p ?o ?g. }
- W3049145469 abstract "Abstract Oxylipins are potent mediators requiring strict control. How they are removed en masse during infection/inflammation is unknown. Herein, lipopolysaccharide (LPS) dynamically increased their mitochondrial β-oxidation, impacting leukocyte bioactivity. Genetic/pharmacological targeting of CPT1 showed <50 oxylipins were robustly removed by macrophage mitochondria during inflammation in vitros and in vivo . Stable isotope-lipidomics demonstrated secretion-reuptake recycling for 12-HETE and its intermediate metabolites. Oxylipin β-oxidation was uncoupled from oxidative phosphorylation. Transcriptional interrogation of human neonatal sepsis revealed significant upregulation of many candidates, encoding proteins for mitochondrial uptake and β-oxidation of long-chain fatty acyls ( ACSL1,3,4 , ACADVL , CPT1B, CPT2 , HADHB) . ACSL1/Acsl1 upregulation was a signature in multiple human/murine macrophage datasets. In summary, mitochondrial β-oxidation is a regulatory metabolic checkpoint for oxylipins during infection. This has implications for patients with CPT1 deficiency, at higher risk of mortality during respiratory infections. We propose that mitochondrial β-oxidation capacity to remove oxylipins during infection may directly influence development of inflammation." @default.
- W3049145469 created "2020-08-21" @default.
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- W3049145469 date "2020-08-18" @default.
- W3049145469 modified "2023-09-25" @default.
- W3049145469 title "Oxylipin metabolism is controlled by mitochondrial β-oxidation during bacterial inflammation" @default.
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