Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I

Eur Heart J. 2013 Aug;34(31):2436-43. doi: 10.1093/eurheartj/eht149. Epub 2013 May 2.


Hyperglycemia and insulin resistance are key players in the development of atherosclerosis and its complications. A large body of evidence suggest that metabolic abnormalities cause overproduction of reactive oxygen species (ROS). In turn, ROS, via endothelial dysfunction and inflammation, play a major role in precipitating diabetic vascular disease. A better understanding of ROS-generating pathways may provide the basis to develop novel therapeutic strategies against vascular complications in this setting. Part I of this review will focus on the most current advances in the pathophysiological mechanisms of vascular disease: (i) emerging role of endothelium in obesity-induced insulin resistance; (ii) hyperglycemia-dependent microRNAs deregulation and impairment of vascular repair capacities; (iii) alterations of coagulation, platelet reactivity, and microparticle release; (iv) epigenetic-driven transcription of ROS-generating and proinflammatory genes. Taken together these novel insights point to the development of mechanism-based therapeutic strategies as a promising option to prevent cardiovascular complications in diabetes.

Keywords: Diabetes; Pathophysiology; Vascular disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Atherosclerosis / etiology
  • Atherosclerosis / metabolism
  • Diabetes Mellitus, Type 2 / etiology*
  • Diabetic Angiopathies / etiology*
  • Diabetic Angiopathies / metabolism
  • Endothelium, Vascular / physiopathology
  • Humans
  • Hyperglycemia / etiology
  • Hyperglycemia / metabolism
  • Insulin Resistance / physiology*
  • Mice
  • MicroRNAs / physiology
  • Nitric Oxide / physiology
  • Obesity / complications
  • Obesity / metabolism
  • Oxidative Stress / physiology
  • Platelet Aggregation / physiology
  • Reactive Oxygen Species / metabolism
  • Thrombosis / etiology
  • Thrombosis / metabolism


  • MicroRNAs
  • Reactive Oxygen Species
  • Nitric Oxide