膜微粒（Microparticles，MP）由于其细胞间信号传递作用参与了心血管疾病过程，但其真正的作用机制尚不完全明确，要点在于其启动病理过程释放的MP如何纳入到靶细胞（心肌细胞和间质细胞）、是否有靶细胞选择性。我们的前期研究不仅发现心衰心肌重构中MP显著升高，也发现PS(Phosphati-dylserine)/PSR与MP纳入靶细胞有重要关系，但需进一步明确病理情况下MP的纳入途径、纳入效率是否有所改变；MP内含因子的整体打包与孤立作用的区别。病理情况下PS/PSR、Annexin V在心血管组织靶细胞表面明显增加，理论上有利于病理性MP纳入到靶细胞。因此，把它们作为研究在病理情况下对MP纳入靶细胞特点的起始点。以细胞培养、心衰心肌重构动物模型为基础，研究病理状态下MP参与心衰过程的特点。并用抗体封闭、抑制PS表达的方法逆向验证。为减少MP对心肌组织病理损伤、寻求治疗方法。

Microparticles（MP）are now known to play important biological effector for cardiac dysfunctions. Circulating levels, both quantitative and qualitative, of MPs are thought to be a reflective index of cardiovascular competence. Therefore, studies to understand the biological relevance of the various permutations and combinations of circulating MPs, their cellular origin and bioactive cargo may lead to increased understanding of the sequelae of CVD and associated diseases. Their biogenesis and release are as a result highly regulated processes in response to cellular activation. PS(Phosphati-dylserine)/PSR, Annexin V are now known to play a crucial role in micro-particles internalization. However, the pathway related PS/PSR for MP internalization in pathobiological status are unclear. Infact, there are more PS/PSR, Annexin V expressing on cell surface in mycaridum tissue. This makes MP internalization theoretical easy. Consequently, there are active interest in the initiation and potentiation of various pathologies. So, we focus on the role of PS/PSR, Annexin V to research the feature MP internalization in cardiac-dysfunction. Aim to understand the role of MPs in cardiovascular disease, look for a new therapy approach of cardiovascular disease in future.