Diabetes and Vascular Disease: Basic Concepts of Nitric Oxide Physiology, Endothelial Dysfunction, Oxidative Stress and Therapeutic Possibilities

Abstract

The vascular manifestations associated with diabetes mellitus (DM) result from the dysfunction of several vascular physiology components mainly involving the endothelium, vascular smooth muscle and platelets. It is also known that hyperglycemia-induced oxidative stress plays a role in the development of this dysfunction. This review considers the basic physiology of the endothelium, especially related to the synthesis and function of nitric oxide. We also discuss the pathophysiology of vascular disease associated with DM. This includes the role of hyperglycemia in the induction of oxidative stress and the role of advanced glycation end-products. We also consider therapeutic strategies.

Ferulic acid combined with astragaloside IV protects against vascular endothelial dysfunction in diabetic rats

“…It is well-known that hyperglycemia-induced oxidative stress and inflammation play an important role in development of vascular endothelial dysfunction (5). Hyperglycemia stimulates the body to produce a large number of oxygen free radicals and then induces oxidative stress which damages vascular endothelial cells and causes DM vascular complications (6).…”

Tonic Inhibition by G Protein–Coupled Receptor Kinase 2 of Akt/Endothelial Nitric-Oxide Synthase Signaling in Human Vascular Endothelial Cells under Conditions of Hyperglycemia with High Insulin Levels

“…In particular, subjects with type 2 diabetes mellitus, which is characterized by insulin resistance, are at 2-to 4-fold increased risk of cardiovascular disease compared with those without diabetes (Kirpichnikov and Sowers, 2001). Vascular endothelial cells play a major role in maintaining cardiovascular homeostasis, and endothelial dysfunction is regarded as an important factor in the pathogenesis of diabetic vascular complications (Capellini et al, 2010). Insulin resistance is associated with endothelial dysfunction.…”

DL-3-n-butylphthalide protects endothelial cells against advanced glycation end product-induced injury by attenuating oxidative stress and inflammation responses

“…Advanced glycation end products (AGEs) are produced by the non-enzymatic glycation and oxidation reactions of glucose or other reducing sugars with proteins, lipids and nucleotides. It had been suggested that AGEs trigger and aggravate the endothelium damage in diabetic complications (2). Previous evidence has linked AGEs with the development of atherosclerosis in diabetes, regardless of the diabetic status (3).…”