Scan Science and Technology
Contact Leading Edge Experts & Companies
The Experts below are selected from a list of 10305 Experts worldwide ranked by ideXlab platform
Stefanie M. Bode-böger – 1st expert on this subject based on the ideXlab platform
Asymmetric Dimethylarginine Accelerates Cellular SenescenceTumor 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.
Nitric Oxide-Asymmetric Dimethylarginine System in Endothelial Cell SenescenceNitric 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.
Response of Asymmetric Dimethylarginine to Hemodialysis-Associated Hypotension in End-Stage Renal Disease PatientsNephron 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
Johann Bauersachs – 2nd expert on this subject based on the ideXlab platform
suppression of endothelial progenitor cells in human coronary artery disease by the endogenous nitric oxide synthase inhibitor Asymmetric DimethylarginineJournal 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 – 3rd expert on this subject based on the ideXlab platform
plasma concentrations of Asymmetric Dimethylarginine a natural inhibitor of nitric oxide synthase in normal pregnancy and preeclampsiaAmerican 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