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机构地区:[1]江苏大学附属医院烧伤整形科,江苏镇江212001
出 处:《中华危重病急救医学》2016年第2期180-183,共4页Chinese Critical Care Medicine
基 金:国家自然科学基金(81272148,81071546,81471903);江苏省自然科学基金(BK2012703)
摘 要:血管内皮细胞(EC)与平滑肌细胞(SMC)是炎症反应中的靶细胞及效应细胞,其结构和功能异常在微循环障碍、脓毒性休克及多器官功能损伤中起着重要作用。本综述回顾了脓毒症时血管EC和SMC的结构功能改变及EC/SMC双向调节作用的相关研究进展,揭示了血管EC和SMC介导的细胞间信号传递对脓毒症的发生发展具有重要的意义。EC和SMC的旁分泌及自分泌构成了细胞间相互调节的网络,改善血管EC和SMC有可能加强对循环系统的控制,支持血流动力学,恢复组织灌注,使细胞代谢正常化,从而降低脓毒症患者的病死率,但具体机制尚有待进一步阐明。Vascular endothelial cells (EC) and smooth muscle cells (SMC) are target and effecter cells of inflammation, and they play an important role in inflammatory responses. The abnormal structure and function of EC and SMC play a significant role in microcirculation disturbance in septic shock and multiple organ dysfunction. This review was meant to discuss the changes in structure and function of EC and SMC and their bidirectional regulation. The cellular linkage of EC and SMC is essential for the interactions between them, and it contributes to the course of sepsis. Paracrine and autocrine as produced by EC and SMC constitute a network for mutual adjustment. Replication of the interaction between EC and SMC facilitates the potential to support hemodynamics, tissue perfusion and cellular metabolism, thereby lower the mortality rate of sepsis. However, the detailed and specific mechanisms remain to be disclosed.
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