Endothelial cell dysfunction and the pathogenesis of diabetic macroangiopathy.

作者: David W. Laight , Martin J. Carrier , Erik E. Änggård

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

关键词:

摘要: 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 morbidity. While many cardiovascular factors are common both atherosclerosis DM, enhanced macroangiopathy may be attributable additional pro-atherogenic mediators associated with insulin resistance syndrome. Given central pathogenic role endotheliopathy in atherosclerosis, it is likely that this vascular monolayer ultimate target injury response such mediators. Furthermore, pro-oxidative, dysfunctional endothelium actively contribute environment through an inappropriate regulation tone, permeability, coagulation, fibrinolysis, cell adhesion proliferation. Such dysfunction mediate hypertension, dyslipidaemia altered haemostasis, addition aggravating vivo resistance.

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