造血干细胞的归巢与缺血性心脏病

Hematopoietic Stem Cells Homing and Ischemic Heart Disease

心肌缺血、缺氧能引起外周血中造血干细胞数量增加及其细胞因子水平增高。CD3+4细胞可向梗死区迁移,并黏附、定位于梗死区,在其细胞因子作用下共同参与梗死区心肌组织修复。在生理和病理情况下这种自我修复的作用较弱,如能利用干细胞技术提高外周血中的CD34+细胞数量,促进其向梗死区归巢,则可增强梗死区组织的修复作用,达到再生心肌与血管的目的。

The myocardial ischacmia and hypoxia could increase the number of the periphera blood stem cells and the production of cytokine. The CD34^＋ cells can migrate to infarcted section and attach as well as locate this section, and then participate the tissue repair in infarcted area under the effect of its cytokines. This kind of repair in physiology and pathology is very weak. If we could advance the amount of the CD34^＋, cells and accelerate its homing to the infract sections through the stem cells technique,we can increase the tissue repair in infarcted area and achieved myocardial and vascular regeneration.