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Although the interaction between endothelial dysfunction and vascular complications of diabetes is not fully understood, the existing view shows that a high glucose environment leads to the impairment of endothelium-dependent vasodilation capacity by increasing oxidative stress and inflammation, reducing vasodilation factor activity, increasing reactive oxygen species (ROS) production, promoting the uncoupling of endothelial nitric oxide synthase (eNOS), and so on ( Figure 2 )

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