S
Sergey Dikalov
Researcher at Vanderbilt University Medical Center
Publications - 203
Citations - 22112
Sergey Dikalov is an academic researcher from Vanderbilt University Medical Center. The author has contributed to research in topics: Superoxide & Oxidative stress. The author has an hindex of 67, co-authored 179 publications receiving 19730 citations. Previous affiliations of Sergey Dikalov include National Institutes of Health & The Wallace H. Coulter Department of Biomedical Engineering.
Papers
More filters
Journal ArticleDOI
Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension
Ulf Landmesser,Sergey Dikalov,S. Russ Price,Louise McCann,Tohru Fukai,Steven M. Holland,William E. Mitch,David G. Harrison +7 more
TL;DR: Evidence is obtained that hypertension produces a cascade involving production of ROSs from the NADPH oxidase leading to oxidation of tetrahydrobiopterin and uncoupling of endothelial NO synthase (eNOS), which decreases NO production and increases ROS production from eNOS.
Journal ArticleDOI
Role of the T cell in the genesis of angiotensin II–induced hypertension and vascular dysfunction
Tomasz J. Guzik,Nyssa E. Hoch,Kathryn A. Brown,Louise McCann,Ayaz Rahman,Sergey Dikalov,Jörg J. Goronzy,Cornelia M. Weyand,David G. Harrison +8 more
TL;DR: A previously undefined role for T cells in the genesis of hypertension is identified and a role of inflammation in the basis of this prevalent disease isSupporting a novel therapeutic target for the treatment of high blood pressure.
Journal ArticleDOI
NAD(P)H Oxidase 4 Mediates Transforming Growth Factor-β1-Induced Differentiation of Cardiac Fibroblasts Into Myofibroblasts
Ioan Cucoranu,Roza E. Clempus,Anna Dikalova,Patrick J. Phelan,Srividya Ariyan,Sergey Dikalov,Dan Sorescu +6 more
TL;DR: It is concluded that Nox 4 mediates TGF-β1–induced conversion of fibroblast to myofibroblasts by regulating Smad 2/3 activation and may play a critical role in the pathological activation of cardiac fibro Blasts in cardiac fibrosis associated with human heart failure.
Journal ArticleDOI
Cross talk between mitochondria and NADPH oxidases
TL;DR: It has been demonstrated that mitochondria-targeted antioxidants break this vicious cycle of ROS production by mitochondria and reducing NADPH oxidase activity, providing a novel strategy for treatment of many pathological conditions including aging, atherosclerosis, diabetes, hypertension, and degenerative neurological disorders in which mitochondrial oxidative stress seems to play a role.
Journal ArticleDOI
Interactions of peroxynitrite, tetrahydrobiopterin, ascorbic acid, and thiols: implications for uncoupling endothelial nitric-oxide synthase.
TL;DR: It is confirmed that ONOO– uncouples eNOS by oxidation of tetrahydrobiopterin and that ascorbate does not fully protect BH4 from oxidation but recycles its radical, and that the BH 4 reaction rate constant exceeds those of thiols or asCorbate.