title: Evolving role of microparticles in the pathophysiology of endothelial dysfunction.
abstract: BACKGROUND
  Endothelial dysfunction is an early event in the development and progression of a wide range of cardiovascular diseases. Various human studies have identified that measures of endothelial dysfunction may offer prognostic information with respect to vascular events. Microparticles (MPs) are a heterogeneous population of small membrane fragments shed from various cell types. The endothelium is one of the primary targets of circulating MPs, and MPs isolated from blood have been considered biomarkers of vascular injury and inflammation.
  
  
  BACKGROUND
  This review summarizes current knowledge of the potential functional role of circulating MPs in promoting endothelial dysfunction. Cells exposed to different stimuli such as shear stress, physiological agonists, proapoptotic stimulation, or damage release MPs, which contribute to endothelial dysfunction and the development of cardiovascular diseases. Numerous studies indicate that MPs may trigger endothelial dysfunction by disrupting production of nitric oxide release from vascular endothelial cells and subsequently modifying vascular tone. Circulating MPs affect both proinflammatory and proatherosclerotic processes in endothelial cells. In addition, MPs can promote coagulation and inflammation or alter angiogenesis and apoptosis in endothelial cells.
  
  
  CONCLUSIONS
  MPs play an important role in promoting endothelial dysfunction and may prove to be true biomarkers of disease state and progression.
authors.affiliation: Division of Cardiac Surgery, Keenan Research Centre in the Li Ka Shing Knowledge Institute at St. Michael's Hospital, Toronto, Ontario, Canada.
authors.forename: Fina
authors.initials: F
authors.lastname: Lovren
authors.forename: Subodh
authors.initials: S
authors.lastname: Verma
mesh_terms: D017209:Apoptosis; D050197:Atherosclerosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D049109:Cell Proliferation; D002470:Cell Survival; D055252:Cell-Derived Microparticles / Q000502:physiology*; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism; D018919:Neovascularization, Physiologic; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress
chemical_list: D009569:Nitric Oxide