Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I.
Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I.
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DOI：
10.1093/eurheartj/eht149
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发表时间：
2013-08
影响因子：
39.3
通讯作者：
Cosentino F
中科院分区：
文献类型：
--
作者：
Paneni F;Beckman JA;Creager MA;Cosentino F
高血糖和胰岛素抵抗是动脉粥样硬化及其并发症发生的关键因素。大量证据表明，代谢异常会导致活性氧（ROS）的过量产生。反过来，ROS通过内皮功能障碍和炎症，在糖尿病血管疾病的沉淀中起主要作用。更好地了解ros生成途径可能为开发针对这种情况下血管并发症的新治疗策略提供基础。本文将重点介绍血管疾病病理生理机制的最新进展：(1)内皮在肥胖诱导的胰岛素抵抗中的新作用；（ii）高血糖依赖的microrna失调和血管修复能力受损；（iii）凝血、血小板反应性和微粒释放的改变；（iv） ros生成和促炎基因的表观遗传驱动转录。综上所述，这些新颖的见解表明，基于机制的治疗策略的发展是预防糖尿病心血管并发症的一个有希望的选择。
Hyperglycemia and insulin resistance are key players in the development of atherosclerosis and its complications. A large body of evidence suggest that metabolic abnormalities cause overproduction of reactive oxygen species (ROS). In turn, ROS, via endothelial dysfunction and inflammation, play a major role in precipitating diabetic vascular disease. A better understanding of ROS-generating pathways may provide the basis to develop novel therapeutic strategies against vascular complications in this setting. Part I of this review will focus on the most current advances in the pathophysiological mechanisms of vascular disease: (i) emerging role of endothelium in obesity-induced insulin resistance; (ii) hyperglycemia-dependent microRNAs deregulation and impairment of vascular repair capacities; (iii) alterations of coagulation, platelet reactivity, and microparticle release; (iv) epigenetic-driven transcription of ROS-generating and proinflammatory genes. Taken together these novel insights point to the development of mechanism-based therapeutic strategies as a promising option to prevent cardiovascular complications in diabetes.
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