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lüll Electrophilic nitro-fatty acids: anti-inflammatory mediators in the vascular compartment Khoo NK; Freeman BACurr Opin Pharmacol 2010[Apr]; 10 (2): 179-84Vascular inflammatory disorders are often associated with both decreased NO bioavailability and a lack of responsiveness to NO, a consequence of impaired NO biosynthesis, dysregulated l-arginine metabolism, endothelial nitric oxide synthase (eNOS) uncoupling and NO consumption induced by redox reactions of NO. The latter is mediated via oxidative inflammatory conditions altering NO-dependent endothelial function, including vascular tone and cell proliferation. The redox reactions of NO and byproducts such as nitrite can react to yield electrophilic nitro-fatty acid derivatives (NO(2)-FAs) and exemplify a biochemical convergence of reactions participating in NO and lipid signaling. NO(2)-FAs represent a novel therapeutic strategy to treat vascular disorders by improving endothelial dysfunction through enhancing NO signaling and blocking vascular smooth muscle proliferation, inflammation, and maladaptive remodeling.|Animals[MESH]|Cardiovascular Diseases/*drug therapy/metabolism[MESH]|Cell Proliferation/drug effects[MESH]|Endothelium, Vascular/drug effects/*metabolism[MESH]|Fatty Acids/chemistry/*metabolism[MESH]|Heme Oxygenase-1/metabolism[MESH]|Humans[MESH]|Inflammation/*drug therapy/metabolism[MESH]|Models, Biological[MESH]|NF-E2-Related Factor 2/metabolism[MESH]|Nitric Oxide Synthase Type III/metabolism[MESH]|Nitric Oxide/chemistry/metabolism[MESH]|Nitro Compounds/*metabolism/pharmacology/*therapeutic use[MESH]|Peroxisome Proliferator-Activated Receptors/agonists[MESH] |