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Stefanie M. Bode-böger - One of the best experts on this subject based on the ideXlab platform.
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Asymmetric Dimethylarginine Accelerates Cellular Senescence
Tumor Dormancy Quiescence and Senescence Volume 2, 2013Co-Authors: Fortunato Scalera, Stefanie M. Bode-bögerAbstract:Cellular senescence, a physiological state of irreversible growth arrest, might contribute to cardiovascular diseases in the elderly. Cellular senescence can be modulated by several different endogenous and exogenous factors that contribute to delay or accelerate the process of senescence. Nitric oxide (NO), formed from L-arginine by nitric oxide synthase (NOS), has antiatherogenic properties and is one of endogenous factors leading to delayed cellular senescence. Intracellular factors that decrease NO synthesis may therefore represent important targets in the accelerated cellular senescence and consequently in the development of cardiovascular diseases. Long-term treatment of human endothelial cells with Asymmetric Dimethylarginine (ADMA), an endogenous competitive inhibitor of NOS and regarded as a novel cardiovascular risk factor, accelerates the process of cellular senescence by inhibiting NO synthesis. Additionally, ADMA accelerates the shortening of telomere length in a dose-dependent manner and inhibits the telomerase activity. Our results suggest a new mechanism through which elevated ADMA levels observed in the elderly might accelerate endothelial senescence and consequently might promote atherogenesis.
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Nitric Oxide-Asymmetric Dimethylarginine System in Endothelial Cell Senescence
Nitric Oxide, 2010Co-Authors: Fortunato Scalera, Stefanie M. Bode-bögerAbstract:This chapter reviews recently accumulating evidence of the nitric oxide (NO)- Asymmetric Dimethylarginine (ADMA) system in the process of endothelial cell senescence and discusses a therapy for regulating the NO-ADMA system. Aging is a major risk factor for development of cardiovascular disease. One of the possible pathophysiological mechanisms through which increasing age may lead to cardiovascular damage is the promotion of endothelial dysfunction via the NO-ADMA system. Senescent human endothelial cells, which produce less NO available for the cGMP signaling cascade and more ADMA, could account for endothelial dysfunction and the development of cardiovascular diseases. Senescence of human endothelial cells can be altered by several different factors that influence the NO-ADMA system, contributing to delay or acceleration of the process of senescence. The close interaction between the NO-ADMA system and biomarkers of endothelial cell senescence suggest that modulation of the NO-ADMA system could influence the process of human endothelial senescence. Therapeutic intervention aimed at preserving bioavailable NO and/or reducing ADMA levels helps to attenuate aging-related cardiovascular diseases. © 2010 Elsevier Inc. All rights reserved.
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Response of Asymmetric Dimethylarginine to Hemodialysis-Associated Hypotension in End-Stage Renal Disease Patients
Nephron Clinical Practice, 2008Co-Authors: Botond Csiky, Endre Sulyok, Jens Martens-lobenhoffer, Orsolya Lakatos, István Wittmann, Stefanie M. Bode-bögerAbstract:Aims: To define the role of Asymmetric Dimethylarginine (ADMA) in the control of blood pressure (BP) during hemodialysis (HD). Methods: L -Argini
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Plasma Asymmetric Dimethylarginine concentration during the perinatal period.
Neonatology, 2007Co-Authors: Gabriella Vida, Endre Sulyok, Tibor Ertl, Jens Martens-lobenhoffer, Stefanie M. Bode-bögerAbstract:Experimental and clinical evidence has been accumulated to indicate that elevated plasma Asymmetric Dimethylarginine (ADMA) levels can be regarded as a marker of endothelial dysfunction that mediates
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Asymmetric Dimethylarginine: A cardiovascular risk factor in renal disease?
Kidney International, 2003Co-Authors: Danilo Fliser, Jan T. Kielstein, Hermann Haller, Stefanie M. Bode-bögerAbstract:Asymmetric Dimethylarginine: A cardiovascular risk factor in renal disease? Endothelial dysfunction due to reduced availability of nitric oxide (NO) is an early step in the course of atherosclerotic vascular disease. NO is synthesized from the amino acid L-arginine by the action of the NO synthase (NOS), which can be blocked by endogenous inhibitors such as Asymmetric Dimethylarginine (ADMA). In laboratory animals, administration of ADMA significantly reduces NO generation, and causes an increase of blood pressure and renal vascular resistance. In clinical studies, a strong correlation between increased ADMA blood levels and impaired endothelial-dependent vasodilatation, and cardiovascular morbidity and mortality has been documented in different populations, including in patients with renal disease. Thus, ADMA seems to be the culprit, and not just an innocent biochemical bystander, of the atherosclerotic disease process. Moreover, reduced NO availability is involved in the progression of renal disease, and increased ADMA blood levels may contribute to this process. Interventions that lower ADMA blood levels in renal patients could, therefore, modulate their atherogenic profile and interfere with progression of renal failure.
Johann Bauersachs - One of the best experts on this subject based on the ideXlab platform.
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suppression of endothelial progenitor cells in human coronary artery disease by the endogenous nitric oxide synthase inhibitor Asymmetric Dimethylarginine
Journal of the American College of Cardiology, 2005Co-Authors: Thomas Thum, Dimitrios Tsikas, Sylvia Stein, Maximilian Schultheiss, Martin Eigenthaler, Stefan D Anker, Philip A Poolewilson, Georg Ertl, Johann BauersachsAbstract:Objectives We tested the hypothesis that Asymmetric Dimethylarginine (ADMA) may be an endogenous inhibitor of endothelial progenitor cells (EPCs). Background Endothelial progenitor cells play a pivotal role in regeneration of injured endothelium, thereby limiting the formation of atherosclerotic lesions. Reduced numbers of EPCs may affect progression of coronary artery disease. Regulation of EPC mobilization and function is mediated in part by nitric oxide (NO). Endogenous inhibitors of NO synthases, such as ADMA, contribute to endothelial dysfunction and injury. Methods We used flow cytometry and in vitro assays to investigate the relationship between EPC number and function with ADMA plasma levels in patients with stable angina. Results The plasma concentration of ADMA was related to the severity of coronary artery disease and correlated inversely with the number of circulating CD34 + /CD133 + progenitor cells (r = −0.69; p Conclusions Asymmetric Dimethylarginine is an endogenous inhibitor of mobilization, differentiation, and function of EPCs. This contributes to the cardiovascular risk in patients with high ADMA levels and may explain low numbers and function of EPCs in patients with coronary artery disease.
S S Nussey - One of the best experts on this subject based on the ideXlab platform.
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plasma concentrations of Asymmetric Dimethylarginine a natural inhibitor of nitric oxide synthase in normal pregnancy and preeclampsia
American Journal of Obstetrics and Gynecology, 1998Co-Authors: Desmond P Holden, S A Fickling, Guy St J Whitley, S S NusseyAbstract:Abstract OBJECTIVE: We investigated the change in the plasma concentration of Asymmetric Dimethylarginine, an endogenous inhibitor of nitric oxide synthase, in early-, mid-, and late-gestation normotensive pregnancies and in gestational age–matched preeclamptic pregnancies and compared the observed changes with changes in blood pressure. STUDY DESIGN: Blood pressure and peripheral plasma Asymmetric Dimethylarginine concentrations were measured in 20 nonpregnant and 145 pregnant women (33 first-trimester, 50 second-trimester, and 44 third-trimester normotensive pregnancies and 18 third-trimester pregnancies complicated by preeclampsia). In 23 normotensive pregnancies serial plasma Asymmetric Dimethylarginine concentrations were measured. Statistical analysis was by analysis of variance and linear regression. RESULTS: The blood pressures recorded throughout normal pregnancy were significantly lower than in nonpregnant subjects (p
Adela Hruby - One of the best experts on this subject based on the ideXlab platform.
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plasma arginine Asymmetric Dimethylarginine ratio and incidence of cardiovascular events a case cohort study
The Journal of Clinical Endocrinology and Metabolism, 2017Co-Authors: Edward Yu, Miguel Ruizcanela, Frank B Hu, Clary B Clish, Dolores Corella, Jordi Salassalvado, Adela HrubyAbstract:Context:Arginine, its methylated metabolites, and other metabolites related to the urea cycle have been independently associated with cardiovascular risk, but the potential causal meaning of these associations (positive for some metabolites and negative for others) remains elusive due to a lack of studies measuring metabolite changes over time. Objective:To examine the association between baseline and 1-year concentrations of urea cycle metabolites and cardiovascular disease (CVD) in a case-cohort setting. Design:A case-cohort study was nested within the Prevencion con Dieta Mediterranea trial. We used liquid chromatography-tandem mass spectrometry to assess metabolite levels at baseline and after 1-year follow-up. The primary CVD outcome was a composite of myocardial infarction, stroke and cardiovascular death. We used weighted Cox regression models (Barlow weights) to estimate multivariable-adjusted hazard ratios (HRs) and their 95% confidence intervals (CIs). Setting:Multicenter randomized trial in Spain. Participants:Participants were 984 participants accruing 231 events over 4.7 years' median follow-up. Main Outcome Measure:Incident CVD. Results:Baseline arginine/Asymmetric Dimethylarginine ratio [HR per standard deviation (SD) = 0.80; 95% CI, 0.67 to 0.96] and global arginine availability [arginine / (ornithine + citrulline)] (HR per SD = 0.83; 95% CI, 0.69 to 1.00) were significantly associated with lower risk of CVD. We observed no significant association for 1-year changes in these ratios or any effect modification by the Mediterranean diet (MD) intervention. Conclusions:A higher baseline arginine/Asymmetric Dimethylarginine ratio was associated with lower CVD incidence in a high cardiovascular risk population. The intervention with the MD did not change 1-year levels of these metabolites.
Rainer H Boger - One of the best experts on this subject based on the ideXlab platform.
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Asymmetric Dimethylarginine adma a novel risk marker in cardiovascular medicine and beyond
Annals of Medicine, 2006Co-Authors: Rainer H BogerAbstract:There is abundant evidence that the endothelium plays a crucial role in the maintenance of vascular tone and structure. One of the major endothelium‐derived vasoactive mediators is nitric oxide (NO), an endogenous messenger molecule formed in healthy vascular endothelium from the amino acid precursor L‐arginine. Endothelial dysfunction is caused by various cardiovascular risk factors, metabolic diseases, and systemic or local inflammation. One mechanism that explains the occurrence of endothelial dysfunction is the presence of elevated blood levels of Asymmetric Dimethylarginine (ADMA) – an L‐arginine analogue that inhibits NO formation and thereby can impair vascular function. Supplementation with L‐arginine has been shown to restore vascular function and to improve the clinical symptoms of various diseases associated with vascular dysfunction.