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
Hauptverfasser: Reeves, Andrew R., Sansbury, Brian E., Pan, Meixia, Han, Xianlin, Spite, Matthew, Greenberg, Andrew S.
Format: Artikel
Sprache:eng
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