微粒在动脉粥样硬化形成及凝血异常中的作用

Roles of Microparticles in the Development and Coagulant Function Abnormality of Atherosclerosis

微粒是血管内皮细胞、组织细胞或血细胞激活或凋亡时形成的亚微型囊泡。动脉粥样硬化时血浆及粥样斑块中富含多种细胞来源的微粒,不仅促进斑块的发生发展并且在动脉粥样硬化凝血异常中起重要作用,可增进血管内皮细胞和白细胞间的相互作用,使单核细胞粘附于内皮细胞,从而迁移到斑块内,吞噬清除内膜下沉积的脂质。巨噬细胞吞噬脂质后凋亡形成大量微粒,抑制内皮细胞合成释放一氧化氮,加重内皮细胞损伤,促进斑块扩大。微粒表面富含的磷脂酰丝氨酸和组织因子是微粒促凝活性的主要来源,病灶处及循环中存在的大量微粒促进了动脉粥样硬化时凝血异常的发生。本文将就微粒在动脉粥样硬化形成及凝血异常中的作用做一综述。

Microparticles（MPs） are submicron vesicles shed from plasma membranes of vascular endothelial cells（ECs）, tissue cells or blood cells in response to cell activation and/or apoptosis. Plasma and plaque in atherosclerosis are abundant in different origins of MPs, which not only contribute to the progression of this disease but play an important role in coagulant function abnormality.Microparticles facilitate interactions of ECs and leukocytes, making monocytes adherent to ECs and then migrating to the plaque for elimination of lipid. After phagocytosis, macrophages become apoptotic and deliver substantial MPs that inhibit synthesis and release of NO by ECs, rendering further injury to ECs and leading to the amplification of atheromatous plaque. Additionally, phosphatidylserine as well as tissue factor expressed on MPs impart them high procoagulant activity, thereby a great many MPs formed in lesion and circulation may accelerate the development and deteriorate the hemostatic dysfunction of atherosclerosis. In this study, we will make a concrete review about the roles of MPs in the development and the coagulant function abnormality of atherosclerosis.