Conclusions

Taken together, there is good evidence that short- and long-term hyperglycemia cause an activation of NADPH oxidase and the formation of ROI. The endothelium has been demonstrated as one of the major sources of ROI generation. Experimental data from in vitro and in vivo studies clearly show that these ROIs are able to induce a thrombogenic transformation of the vessel wall and to be the cause for the endothelial dysfunction observed in diabetes but also in hypertension and hypercholesterolemia. Whether these cytotoxic effects are exerted by superoxide anions directly or are mediated by peroxynitrite depends on the local environment and the type of vasculature regarded. Our current knowledge is summarized in the hypothesis shown

Glucose/AGE

Apoptosis NF-kB ox-LDL MMP

Figure 6 Current hypothesis: formation of ROI by hyperglycemia and the effects of ROI on the vessel wall as cause for the development of vascular complications in diabetes.

Apoptosis NF-kB ox-LDL MMP

Figure 6 Current hypothesis: formation of ROI by hyperglycemia and the effects of ROI on the vessel wall as cause for the development of vascular complications in diabetes.

in Fig. 6. It is important to recognize that the consequences of these ROI-induced vascular dysfunctions might be different depending on the size of the vasculature affected: In small vessels the oxidative stress induced by hyperglycemia might be one important factor for the stimulation of proliferation of endothelium and the formation of new partially malfunctional vessels and thereby contribute to the development of small vessel disease (retinopathy, nephropathy). In coronary vasculature, the generation of ROI might be more important for the destabilization of atherosclerotic plaques, causing an increased cardiac risk in diabetic patients. The reestablishment of the antioxidative network might therefore be a useful approach to protect the vasculature in diabetes.

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