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糖尿病并发症的炎症机制

Inflammatory mechanisms of diabetic complications.

作者信息

Williams Michael D, Nadler Jerry L

机构信息

Division of Endocrinology and Metabolism, University of Virginia, P.O. Box 801405, 450 Ray C. Hunt Drive, Room 1220, Charlottesville, VA 22908-1405, USA.

出版信息

Curr Diab Rep. 2007 Jun;7(3):242-8. doi: 10.1007/s11892-007-0038-y.

Abstract

Activation of inflammatory processes may contribute to the development of type 2 diabetes mellitus. In addition, inflammation appears to be a major mechanism responsible for vascular damage leading to the clinically well-recognized complications of diabetes. Inflammatory cytokine and chemokine mediators released from visceral fat contribute to atherosclerotic plaque formation and increased risk for myocardial infarction and stroke. Activation of growth factors and adhesion molecules may promote the movement of inflammatory cells into the renal microvasculature, predisposing to the development of diabetic nephropathy. Emerging evidence also indicates that markers of inflammation are associated with the more severe forms of diabetic retinopathy. Future approaches to the treatment of diabetic complications may involve regulation of inflammatory processes, specifically targeting factors that contribute to vascular damage.

摘要

炎症过程的激活可能促使2型糖尿病的发展。此外,炎症似乎是导致糖尿病临床公认并发症的血管损伤的主要机制。内脏脂肪释放的炎性细胞因子和趋化因子介质有助于动脉粥样硬化斑块的形成,并增加心肌梗死和中风的风险。生长因子和黏附分子的激活可能促进炎性细胞进入肾脏微血管,易引发糖尿病肾病。新出现的证据还表明,炎症标志物与更严重形式的糖尿病视网膜病变有关。未来治疗糖尿病并发症的方法可能涉及对炎症过程的调控,特别是针对导致血管损伤的因素。

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