Relevance of endothelial-haemostatic dysfunction in cigarette smoking

Curr Med Chem. 2007;14(17):1887-92. doi: 10.2174/092986707781058832.


Cigarette smoking plays a major role in the development of atherosclerosis and is associated with increased morbidity and mortality for coronary heart disease, stroke and peripheral vascular disease. In spite of the abundance of epidemiological evidence that links cigarette smoking to vascular disease, the pathologic mechanisms for such interaction are not clear. The endothelium is a major target organ that undergoes activation when exposed to common vascular triggers, including hypertension, hypercholesterolemia, hyperglycaemia and smoking. Changes in endothelial function may lead to a dysfunctional vascular phenotype characterized by anomalous responses of the vascular tone, abnormal endothelial proliferation and prothrombotic activation. Several studies have demonstrated that smoking may alter endothelial function by a direct toxic effect and consequently trigger haemostatic activation and thrombosis. In this article we will review the evidence that loss of normal endothelial function may result in a loss of the balance of the haemostatic system and in changes of the platelet physiology that may be relevant for the pathogenic effect of smoking on the development of atherothrombosis.

Publication types

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

MeSH terms

  • Animals
  • Blood Platelets / drug effects
  • Blood Platelets / physiology
  • Cell Adhesion Molecules
  • Endothelium, Vascular / physiopathology*
  • Hemostasis / physiology*
  • Humans
  • Lipoproteins / blood
  • Lipoproteins / metabolism
  • Muscle, Smooth, Vascular / physiopathology
  • Oxidative Stress / physiology
  • Signal Transduction / drug effects
  • Smoking / blood
  • Smoking / physiopathology*


  • Cell Adhesion Molecules
  • Lipoproteins