DHA

Dha is a lipid of Fatty Acyls (FA) class. Dha is associated with abnormalities such as Atherosclerosis, Consumption-archaic term for TB, Chronic disease, Cardiovascular Diseases and Diabetes Mellitus, Non-Insulin-Dependent. The involved functions are known as Inflammation, Oxidation, fatty acid oxidation, Fatty Acid Metabolism and Lipid Metabolism. Dha often locates in Hepatic, Protoplasm, Mucous Membrane, Epithelium and outer membrane. The associated genes with DHA are IMPACT gene, FATE1 gene, GAPDH gene, THOC4 gene and SLC33A1 gene. The related lipids are stearidonic acid, Fatty Acids, Total cholesterol, Lipopolysaccharides and Dietary Fatty Acid. The related experimental models are Mouse Model, Transgenic Model, Animal Disease Models and Arthritis, Experimental.

References related to genes published in FASEB J.


PMIDJournalPublished DateAuthorTitle
21478260FASEB J.2011Hellmann J et al.Resolvin D1 decreases adipose tissue macrophage accumulation and improves insulin sensitivity in obese-diabetic mice.
20833872FASEB J.2011Chen P et al.Poxytrins, a class of oxygenated products from polyunsaturated fatty acids, potently inhibit blood platelet aggregation.
20959515FASEB J.2011Yamada T et al.Eosinophils promote resolution of acute peritonitis by producing proresolving mediators in mice.
19890019FASEB J.2010Gleissman H et al.Docosahexaenoic acid metabolome in neural tumors: identification of cytotoxic intermediates.
17056761FASEB J.2006González-Périz A et al.Docosahexaenoic acid (DHA) blunts liver injury by conversion to protective lipid mediators: protectin D1 and 17S-hydroxy-DHA.
18559988FASEB J.2008Merched AJ et al.Atherosclerosis: evidence for impairment of resolution of vascular inflammation governed by specific lipid mediators.
23504711FASEB J.2013Dalli J et al.The novel 13S,14S-epoxy-maresin is converted by human macrophages to maresin 1 (MaR1), inhibits leukotriene A4 hydrolase (LTA4H), and shifts macrophage phenotype.
23407709FASEB J.2013Miyahara T et al.D-series resolvin attenuates vascular smooth muscle cell activation and neointimal hyperplasia following vascular injury.