Myeloid-specific deficiency of long-chain acyl CoA synthetase 4 (Acsl4) reduces inflammation in vitro and in vivo by remodeling phospholipids and reducing production of arachidonic acid-derived proinflammatory lipid mediators
In response to infection or tissue damage, resident peritoneal macrophages (rpMACs) produce inflammatory lipid mediators from the polyunsaturated fatty acid (PUFA), arachidonic acid (AA). Long-chain acyl-CoA synthetase 4 (ACSL4) catalyzes the covalent addition of a CoA moiety to fatty acids, with a...
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Veröffentlicht in: | The Journal of immunology (1950) 2021-11, Vol.207 (11), p.2744-2753 |
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Format: | Artikel |
Sprache: | eng |
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