| Autor: |
Dowsett L; Institute of Cardiovascular and Medical Sciences, College of Medicine, Veterinary, and Life Sciences, The University of Glasgow, Glasgow G12 8QQ, UK., Higgins E; Institute of Cardiovascular and Medical Sciences, College of Medicine, Veterinary, and Life Sciences, The University of Glasgow, Glasgow G12 8QQ, UK., Alanazi S; Institute of Cardiovascular and Medical Sciences, College of Medicine, Veterinary, and Life Sciences, The University of Glasgow, Glasgow G12 8QQ, UK.; Department of Pharmacology and Toxicology, College of Pharmacy, Al-Jouf University, Sakaka P.O. Box 2014, Saudi Arabia., Alshuwayer NA; Institute of Cardiovascular and Medical Sciences, College of Medicine, Veterinary, and Life Sciences, The University of Glasgow, Glasgow G12 8QQ, UK.; Department of Anatomy, College of Medicine, King Saud University, Riyadh 11451, Saudi Arabia., Leiper FC; Institute of Cardiovascular and Medical Sciences, College of Medicine, Veterinary, and Life Sciences, The University of Glasgow, Glasgow G12 8QQ, UK., Leiper J; Institute of Cardiovascular and Medical Sciences, College of Medicine, Veterinary, and Life Sciences, The University of Glasgow, Glasgow G12 8QQ, UK. |
| Abstrakt: |
Atherosclerosis is a chronic cardiovascular disease which increases risk of major cardiovascular events including myocardial infarction and stroke. Elevated plasma concentrations of asymmetric dimethylarginine (ADMA) have long been recognised as a hallmark of cardiovascular disease and are associated with cardiovascular risk factors including hypertension, obesity and hypertriglyceridemia. In this review, we discuss the clinical literature that link ADMA concentrations to increased risk of the development of atherosclerosis. The formation of atherosclerotic lesions relies on the interplay between vascular dysfunction, leading to endothelial activation and the accumulation of inflammatory cells, particularly macrophages, within the vessel wall. Here, we review the mechanisms through which elevated ADMA contributes to endothelial dysfunction, activation and reactive oxygen species (ROS) production; how ADMA may affect vascular smooth muscle phenotype; and finally whether ADMA plays a regulatory role in the inflammatory processes occurring within the vessel wall. |
