Endothelial microparticles (EMPs) are complex vesicular structures that originate from plasma membranes of activated or apoptotic endothelial cells. EMPs play a significant role in vascular function by altering the processes of inflammation, coagulation, and angiogenesis, and they are key players in the pathogenesis of several vascular diseases. Circulating EMPs are increased in many age-related vascular diseases such as coronary artery disease, peripheral vascular disease, cerebral ischemia, and congestive heart failure. Their elevation in plasma has been considered as both a biomarker and bioactive effector of vascular damage and a target for vascular diseases. This review focuses on the pleiotropic roles of EMPs and the mechanisms that trigger their formation, particularly the involvement of decreased estrogen levels, thrombin, and PAI-1 as major factors that induce EMPs in age-related vascular diseases. 1. Introduction Vascular diseases are among the most common causes of morbidity and mortality, and both number and severity of morbid vascular conditions increase with age. Regulations of angiogenesis, coagulation, and inflammation are very important issues in vascular biology, both in normal physiology and pathology [1]. It is now well established that disruption of endothelial integrity represents a crucial event in the initiation and development of cardiovascular (CV) diseases. Numerous studies have reported that microparticles (MPs) play an important role in endothelial dysfunction. Endothelial dysfunction occurs when a perturbed homeostatic endothelium disrupts vascular competency resulting in reduced vasodilatation and increased proinflammatory and prothrombotic properties of the vascular network [2]. Recently, MPs originating from various cells have been found to be associated with several vascular related diseases. Moreover, exposed procoagulant phospholipids and specific receptors at the surface of MPs act as biomessengers linking inflammation, coagulation, and angiogenesis [3–5]. Although MPs were first described as “cellular debris” that are believed to have no biological significance, recent studies documented that MPs of endothelial and other origins are biological effectors in inflammation, vascular injury, angiogenesis, and thrombosis [6–8]. MPs isolated from granulation tissue are derived from endothelial cells, monocytes, platelets, erythrocytes [9–13], and myofibroblasts [8]. They exchange biological signals and information intercellularly and each kind of MP carries the antigens and receptors of the cells they originated. MPs may
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