Asymmetrical dimethylarginine as a mediator of endothelial dysfunction in acute inflammation at different disease stages

Bibliográfalaš dieđut
Váldodahkkit:	Demosthenous, M, Antoniades, C, Antonopoulos, S, Tousoulis, D, Bakogiannis, C, Vlachopoulos, C, Petrochilou, K, Toutouza, M, Channon, K, Stefanadis, C
Materiálatiipa:	Conference item
Almmustuhtton:	2010

Role of asymmetrical dimethylarginine in inflammation-induced endothelial dysfunction in human atherosclerosis.
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Haplotype on GTP-Cyclohydrolase I Gene, Reveals a Novel Role of Tetrahydrobiopterin as a Defense Mechanism Against Inflammation-Induced Endothelial Dysfunction in Human Atherosclerosis
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Response to Asymmetrical Dimethylarginine, Oxidative Stress, and Atherosclerosis
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Induction of vascular GTP-cyclohydrolase I and endogenous tetrahydrobiopterin synthesis protect against inflammation-induced endothelial dysfunction in human atherosclerosis.
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Induction of vascular GTP-cyclohydrolase i and endogenous tetrahydrobiopterin synthesis protect against inflammation-induced endothelial dysfunction in human atherosclerosis
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Association of plasma asymmetrical dimethylarginine (ADMA) with elevated vascular superoxide production and endothelial nitric oxide synthase uncoupling: implications for endothelial function in human atherosclerosis.
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Acute Inflammation Rapidly Increases Plasma Biopterins and Impairs Endothelial Function: A Novel Role of Plasma Tetrahydrobiopterin as a Marker of Acute Inflammation
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Methionine-induced homocysteinemia impairs endothelial function in hypertensives: the role of asymmetrical dimethylarginine and antioxidant vitamins.
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Asymmetrical dimethylarginine regulates endothelial function in methionine-induced but not in chronic homocystinemia in humans: effect of oxidative stress and proinflammatory cytokines.
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Platelet activation in atherogenesis associated with low-grade inflammation.
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Statin treatment improves vascular redox state through a tetrahydrobiopterin-mediated re-coupling of endothelial nitric oxide synthase, in human atherosclerosis
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The role of adiponectin at different stages of atherosclerosis in heart failure: associations with myocardial redox state
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Evaluation of endothelial function
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Gene therapy for dysfunctional endothelium: is dimethylarginine dimethylaminohydrolase-2 a therapeutic target?
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Study of endothelial dysfunction and asymmetric dimethylarginine levels
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Genetic variability on adiponectin gene affects myocardial infarction risk: the role of endothelial dysfunction.
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Genetic variability on adiponectin gene affects myocardial infarction risk: The role of endothelial dysfunction
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Asymmetric dimethylarginine (ADMA) and endothelial dysfunction: implications for atherogenesis
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Novel therapeutic strategies targeting vascular redox in human atherosclerosis.
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Mechanisms of testosterone deficiency-related endothelial dysfunction: invited commentary for the Hellenic Journal of Cardiology on: Tsikas et al. “Associations between asymmetric dimethylarginine, nitrite-dependent renal carbonic anhydrase activity and plasma testosterone levels in hypogonadal men”
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Short-Term Atorvastatin Treatment Reduces Vascular Oxidative Stress Saphenous Vein Grafts by Improving eNOS Coupling and Reducing NADPH-Oxidase Activity in Patients Undergoing Elective CABG
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Atorvastatin rapidly improves redox state in human vein grafts ex-vivo, by directly reducing NADPH-oxidase activity and improving eNOS coupling
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Atorvastatin rapidly modifies vascular redox state and improves nitric oxide bioavailability in human vessels obtained from patients with advanced atherosclerosis
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Myocardial Redox State Predicts Post-Operative Clinical Outcome in Patients Undergoing Elective CABG: The Role of NADPH-Oxidase and Uncoupled Nitric Oxide Synthase
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Interrelationships between vascular superoxide and adiponectin biosynthesis in perivascular adipose tissue in human atherosclerosis
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Genetic Variability of Adiponectin Gene Defines the Biosynthesis Rate of Adiponectin in Adipose Tissue and Regulates Superoxide Generation in Human Arteries in vivo
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Associations Between Serum Adiponectin, Vascular O2-Generation and NO Bioavailability In Patients With Coronary Atherosclerosis
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Serum adiponectin regulates vascular O2-generation and NO bioavailability in patients with coronary atherosclerosis
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Rapid Effects of Atorvastatin on Tetrahydrobiopterin-Mediated eNOS Coupling in Human Arteries, is Mediated by Stimulation of Vascular GTP-Cyclohydrolase
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Oral Atorvastatin Treatment Improves NO Bioavailability and Vascular Redox State in the Human Arterial Wall, via a Tetrahydrobiopterin-Mediated Improvement of eNOS Coupling
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Preoperative atorvastatin treatment rapidly improves vein graft redox state by inhibiting rac1 and NADPH oxidase activity in patients undergoing elective CABG
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Atorvastatin directly improves vascular redox state by affecting eNOS coupling and NADPH-oxidase activity in human vein grafts ex-vivo
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Hyperuricemia induces endothelial dysfunction and accelerates atherosclerosis by disturbing the asymmetric dimethylarginine/dimethylarginine dimethylaminotransferase 2 pathway
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LOCAL ADIPONECTIN SYNTHESIS IN ADIPOSE TISSUE REGULATES VASCULAR SUPEROXIDE GENERATION IN PATIENTS WITH CORONARY ATHEROSCLEROSIS: INSIGHTS BY USING FUNCTIONAL GENETIC POLYMORPHISMS OF ADIPONECTIN GENE
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Effects of atorvastatin on endothelial function and the expression of proinflammatory cytokines and adhesion molecules in young subjects with successfully repaired coarctation of aorta.
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Effects of atorvastatin on endothelial function and the expression of proinflammatory cytokines and adhesion molecules in young subjects with successfully repaired coarctation of aorta
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Differential responses of distinct adipose tissue depots to acute and chronic inflammation: novel insights into the complex mechanisms regulating adiponectin biosynthesis in humans
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Asymmetrical dimethylarginine as a mediator of endothelial dysfunction in acute inflammation at different disease stages

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