Journal
PROSTAGLANDINS & OTHER LIPID MEDIATORS
Volume 139, Issue -, Pages 48-53Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.prostaglandins.2018.09.008
Keywords
Hypertension; Inflammation; Isolevuglandins
Categories
Funding
- National Institutes of Health [K01HL130497]
- American Heart Association Scientist Development Grant [17SDG33670829]
- National Center for Advancing Translational Sciences [UL1 TR002243]
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Inflammation has been implicated in the pathogenesis of hypertension and recent evidence suggests that isolevuglandin (IsoLG)-protein adducts play a role. Several hypertensive stimuli contribute to formation of IsoLG-protein adducts including excess dietary salt and catecholamines. The precise intracellular mechanisms by which these hypertensive stimuli lead to IsoLG-protein adduct formation are still not well understood; however, there is now evidence implicating NADPH-oxidase derived reactive oxygen species (ROS) in this process. ROS oxidize arachidonic acid leading to formation of IsoLGs, which non-covalently adduct to lysine residues and alter protein structure and function. Recent studies suggest that these altered proteins act as neo-antigens leading to an autoimmune state that results in hypertension. The goal of this mini-review is to highlight some of the hypertensive stimuli and the mechanisms contributing to IsoLG-protein adduct formation leading to inflammation and hypertension.
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