Oxidative damage of the vascular endothelium in type 2 diabetes – the role of mitochondria and NAD(P)H oxidase

Abstract

Endothelial dysfunction is one of the major diabetic complications causing morbidity and mortality of large number of patients. Oxidative stress is key factor in the development and progression of such pathological changes. Hyperglycaemia and/or hyperlipidaemia accompanying diabetes, cause increased production of reactive oxygen species in parallel with significantly reduced antioxidative defence. The vascular endothelium is not only passive lining of the vessels but also highly metabolically active tissue. It produces and secretes a number of factors responsible for the maintenance of vascular homeostasis. Oxidative stress leads to changes in vascular tone, which mainly involves the reduction of NO bioavailability. There are several ROS generating mechanisms, however it seems that the mitochondrial respiratory chain and NAD(P)H oxidase play a most significant role in endothelium. The endothelial dysfunction in diabetes, the importance of mitochondria and NAD(P)H oxidase in the development of pathological changes would be discussed below.