Diabetic vascular complications: pathophysiology, biochemical basis and potential therapeutic strategy

Curr Pharm Des. 2005;11(18):2279-99. doi: 10.2174/1381612054367300.


Diabetic vascular complication is a leading cause of end-stage renal failure, acquired blindness, a variety of neuropathies and accelerated atherosclerosis, which could account for disabilities and high mortality rates in patients with diabetes. Recent large prospective clinical studies have shown that intensive glucose control reduces effectively microvascular complications among patients with diabetes, and insulin resistance and postprandial hyperglycemia seem to be involved in diabetic macrovascular complications. Chronic hyperglycemia is a major initiator of diabetic vascular complications. Indeed, high glucose, via various mechanisms such as increased production of advanced glycation end products, activation of protein kinase C, stimulation of the polyol pathway and enhanced reactive oxygen species generation, regulates vascular inflammation, altered gene expression of growth factors and cytokines, and platelet and macrophage activation, thus playing a central role in the development and progression of diabetic vascular complications. This article summarizes the molecular mechanisms of diabetic vascular complications and the potential therapeutic interventions that may prevent these disorders even in the presence of hyperglycemia, control of which is often difficult with current therapeutic options.

Publication types

  • Review

MeSH terms

  • Animals
  • Diabetic Angiopathies / metabolism
  • Diabetic Angiopathies / physiopathology
  • Diabetic Angiopathies / therapy*
  • Diabetic Nephropathies / metabolism
  • Diabetic Nephropathies / physiopathology
  • Diabetic Nephropathies / therapy
  • Diabetic Neuropathies / metabolism
  • Diabetic Neuropathies / physiopathology
  • Diabetic Neuropathies / therapy
  • Diabetic Retinopathy / metabolism
  • Diabetic Retinopathy / physiopathology
  • Diabetic Retinopathy / therapy
  • Humans