Inflammatory mechanisms of diabetic complications.
Inflammatory mechanisms of diabetic complications.
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DOI：
10.1007/s11892-007-0038-y
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发表时间：
2007-06-01
影响因子：
4.2
通讯作者：
Nadler, Jerry L
中科院分区：
文献类型：
--
作者：
Williams, Michael D;Nadler, Jerry L
炎症过程的激活可能有助于2型糖尿病的发展。此外，炎症似乎是导致血管损伤的主要机制，导致临床上公认的糖尿病并发症。内脏脂肪释放的炎性细胞因子和趋化因子介体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。生长因子和粘附分子的活化可促进炎性细胞向肾微血管的移动，从而诱发糖尿病肾病的发展。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。未来糖尿病并发症的治疗方法可能涉及炎症过程的调节，特别是针对导致血管损伤的因素。
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.