Inflammation in the pathogenesis of microvascular complications in diabetes.
Inflammation in the pathogenesis of microvascular complications in diabetes.
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DOI：
10.3389/fendo.2012.00170
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发表时间：
2012
影响因子：
5.2
通讯作者：
Grant MB
中科院分区：
文献类型：
--
作者：
Nguyen DV;Shaw LC;Grant MB
糖尿病和高血糖会产生促炎性微环境，进而发展为肾病、视网膜病和神经病等微血管并发症。饮食引起的胰岛素抵抗是 2 型糖尿病这种变化的潜在引发因素，它可以增加脂肪因子并产生慢性低度炎症状态。晚期糖基化终末产物及其受体、糖基化终末产物AGE受体轴、活性氧和缺氧也会相互作用，使并发症恶化。人们已经做出了许多努力来了解这些调节剂和减轻炎症反应的机制，但是，仍然没有出现有效的治疗方法。炎症信号传导的复杂性可能表明需要多靶点治疗。这篇综述介绍了针对新治疗策略的最新发现。
Diabetes and hyperglycemia create a proinflammatory microenvironment that progresses to microvascular complications such as nephropathy, retinopathy, and neuropathy. Diet-induced insulin resistance is a potential initiator of this change in type 2 diabetes which can increase adipokines and generate a chronic low-grade inflammatory state. Advanced glycation end-products and its receptor, glycation end-products AGE receptor axis, reactive oxygen species, and hypoxia can also interact to worsen complications. Numerous efforts have gained way to understanding the mechanisms of these modulators and attenuation of the inflammatory response, however, effective treatments have still not emerged. The complexity of inflammatory signaling may suggest a need for multi-targeted therapy. This review presents recent findings aimed at new treatment strategies.