Endothelial cell dysfunction and the pathogenesis of diabetic macroangiopathy

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 e...

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Bibliographic Details
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
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Summary: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.
ISSN:1520-7552
1520-7560
DOI:10.1002/(SICI)1520-7560(199907/08)15:4<274::AID-DMRR46>3.0.CO;2-G