Endothelial cell dysfunction and the pathogenesis of diabetic macroangiopathy

• Published in: Diabetes/metabolism research and reviews 1999-07, Vol.15 (4), p.274-282
• Main Authors: Laight, David W., Carrier, Martin J., Änggård, Erik E.
• Format: Article
• Language: English
• Subjects: angiopathy; Arteriosclerosis - etiology; Associated diseases and complications; atherosclerosis; Biological and medical sciences; Diabetes Mellitus, Type 2 - physiopathology; Diabetes. Impaired glucose tolerance; Diabetic Angiopathies - etiology; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; endothelium; Endothelium, Vascular - physiopathology; Humans; Insulin Resistance; Medical sciences; nitric oxide; oxidant stress; Oxidative Stress
• ISSN: 1520-7552; 1520-7560
• DOI: 10.1002/(SICI)1520-7560(199907/08)15:4<274::AID-DMRR46>3.0.CO;2-G

Type 2 diabetes mellitus (DM) represents a high risk condition for the development of atherosclerotic and thromboembolic macroangiopathy, which make major contributions to diabetic mortality and morbidity. While many cardiovascular risk factors are common to both atherosclerosis and Type 2 DM, the enhanced risk of diabetic macroangiopathy may be attributable to additional pro‐atherogenic mediators associated with insulin resistance syndrome. Given the central pathogenic role of endotheliopathy in atherosclerosis, it is likely that this vascular monolayer is the ultimate target of injury in response to such mediators. Furthermore, a pro‐oxidative, dysfunctional endothelium may actively contribute to the pro‐atherogenic environment through an inappropriate regulation of vascular tone, permeability, coagulation, fibrinolysis, cell adhesion and proliferation. Such dysfunction may mediate hypertension, dyslipidaemia and altered haemostasis, in addition to aggravating in vivo insulin resistance. Copyright © 1999 John Wiley & Sons, Ltd.