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药物治疗能否逆转糖尿病患者内皮祖细胞功能障碍?

Does drug therapy reverse endothelial progenitor cell dysfunction in diabetes?

机构信息

Omaha VA Medical Center, Omaha, NE, USA; University of Nebraska Medical Center, Omaha, NE, USA.

出版信息

J Diabetes Complications. 2013 Sep-Oct;27(5):519-25. doi: 10.1016/j.jdiacomp.2013.04.007. Epub 2013 Jul 1.

DOI:10.1016/j.jdiacomp.2013.04.007
PMID:23809765
Abstract

Endothelial progenitor cells (EPCs) are vital for the maintenance and repair of the endothelium. Decreased EPC number and function have been associated with increased cardiovascular (CVD) risk. Patients with diabetes have decreased number of circulating EPCs and decreased EPC function. This may account for some of the increased CVD risk seen in patients with diabetes that is not explained by traditional risk factors such as glycemic control, dyslipidemia and hypertension. Recent studies seem to indicate that drugs commonly used in diabetes patients such as metformin, thiazolidinediones, GLP-1 agonists, DPP-4 inhibitors, insulin, statins and ACE inhibitors may increase EPC number and improve EPC function. The mechanisms by which these drugs modulate EPC function may involve reduction in inflammation, oxidative stress and insulin resistance as well as an increase in nitric oxide (NO) bioavailability. This review will discuss the evidence in the literature regarding the above mentioned topics.

摘要

内皮祖细胞 (EPCs) 对于维持和修复内皮至关重要。EPC 数量和功能的减少与心血管疾病 (CVD) 风险的增加有关。糖尿病患者循环中的 EPC 数量减少,EPC 功能降低。这可能解释了部分糖尿病患者 CVD 风险增加的原因,而这些风险无法用传统的危险因素(如血糖控制、血脂异常和高血压)来解释。最近的研究似乎表明,糖尿病患者常用的药物,如二甲双胍、噻唑烷二酮类、GLP-1 激动剂、DPP-4 抑制剂、胰岛素、他汀类药物和 ACE 抑制剂,可能会增加 EPC 数量并改善 EPC 功能。这些药物调节 EPC 功能的机制可能涉及减少炎症、氧化应激和胰岛素抵抗,以及增加一氧化氮 (NO) 的生物利用度。本文将讨论文献中关于上述主题的证据。

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Does drug therapy reverse endothelial progenitor cell dysfunction in diabetes?药物治疗能否逆转糖尿病患者内皮祖细胞功能障碍?
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