糖尿病引起内皮祖细胞损伤机制研究进展

The underlying mechanisms of dysfunction of endothelial progenitor cells caused by diabetes

内皮祖细胞来源于骨髓细胞，在维持内皮细胞完整性和缺血组织的血管新生方面起关键作用。糖尿病可引起内皮祖细胞功能障碍，其机制包括促进活性氧簇产生，降低内皮型一氧化氮合酶活性，刺激炎性反应，抑制与血管新生有关的蛋白信号通路等，最终导致血管新生障碍，这是糖尿病患者出现心血管并发症、伤口愈合延迟甚至面临截肢危险的重要原因。探索作用于受损糖尿病内皮祖细胞功能的新靶点，可通过改善内皮祖细胞功能，开拓治疗糖尿病心血管病变和足病的新途径。

Endothelial progenitor cells （EPCs） derived from bone marrow,play crucial roles in the maintenance of endothelial cell integrity and in the neovascularization of ischemic tissue. The mechanisms of EPCs impairment in diabetes include increased production of reactive oxygen species, reduced bioavailability of endothelial nitric oxide synthase, activated process of inflammation and inhibited signaling pathways of an- giogenesis related proteins. These multiple abnormalities contribute to defective angiogenesis, resulting in car- diovascular complications, delayed wound healing and ascending risk of lower limb amputation in diabetes. By exploring new targets acting on dysfunction of diabetic EPCs, new approaches to prevent and cure cardiovas- cular events and foot disorders could be found through improving EPCs function in patients with diabetes.