甲基乙二醛
糖基化
糖尿病
促炎细胞因子
乙二醛
发病机制
肾病
氧化应激
糖尿病肾病
医学
化学
药理学
生物信息学
免疫学
生物化学
内分泌学
生物
酶
炎症
有机化学
作者
Sultan Alouffi,Mohd Shahnawaz Khan
出处
期刊:Current Protein & Peptide Science
[Bentham Science Publishers]
日期:2020-08-31
卷期号:21 (9): 890-898
被引量:1
标识
DOI:10.2174/1389203720666191010155145
摘要
It has been well established that advanced glycation end-products (AGEs) have a strong correlation with diabetes and its secondary complications. Moreover, dicarbonyls, especially, methylglyoxal (MG) and glyoxal, accelerate AGEs formation and hence, have potential roles in the pathogenesis of diabetes. They can also induce oxidative stress and concomitantly decrease the efficiency of antioxidant enzymes. Increased proinflammatory cytokines (tumor necrosis factor-α and interleukin- 1β) are secreted by monocytes due to the dicarbonyl-modified proteins. High levels of blood dicarbonyls have been identified in diabetes and its associated complications (retinopathy, nephropathy and neuropathy). This review aims to provide a better understanding by including in-depth information about the formation of MG and glyoxal through multiple pathways with a focus on their biological functions and detoxifications. The potential role of these dicarbonyls in secondary diabetic complications is also discussed.
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