動脈硬化と血管内皮障害(<特集>動脈硬化とアフェレシス)

概要

論文の詳細を見る
In recent years, it has become clear that insulin resistance and endothelial dysfunction play a central role in the pathogenesis of atherosclerosis. Endothelial dysfunction associated with metabolic syndrome and other insulin-resistant states is characterized by impaired insulin-stimulated nitric oxide (NO) production from the endothelium. The down-regulation of the antiatherogenic phosphatidylinositol-3-kinase-mediated insulin receptor-signaling pathway, and maintained activity of the proatherogenic mitogenic-activated protein kinase pathway in insulin-resistant states, leads to accelerated atherosclerosis. NO deficiency results from decreased synthesis and/or release, in combination with exaggerated consumption in tissues by high levels of reactive oxygen (ROS), which are produced by cellular disturbances in glucose and lipid metabolism. Vascular damage, which results from lipid deposition and oxidative stress to the vessel wall, triggers an inflammatory reaction, and the release of chemoattractants and cytokines worsens the insulin resistance and endothelial dysfunction. An increased release of free fatty acids (FFAs) and TNF-α from adipocytes block the insulin signal transcription pathway and induce endothelial dysfunction. Tiazolidinediones (TZDs) are agonists of peroxisome proliferator-activated receptor (PPAR)-γ, and decrease circulating FFA and TNF-α and increase adiponectin concentration. From the clinical standpoint, much experimental evidence supports the concept that therapies that improve insulin resistance and endothelial dysfunction reduce cardiovascular morbidity and mortality.
日本アフェレシス学会の論文
2008-02-29

動脈硬化と血管内皮障害(<特集>動脈硬化とアフェレシス)

スポンサーリンク

概要

著者

関連論文

スポンサーリンク