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糖基化氧化与 2 型糖尿病心血管并发症:临床更新。

Glyco-oxidation and cardiovascular complications in type 2 diabetes: a clinical update.

机构信息

Department of Medicine - DIMED, University of Padova, Via dei Colli 4, 35143, Padua, Italy.

出版信息

Acta Diabetol. 2013 Apr;50(2):101-10. doi: 10.1007/s00592-012-0412-3. Epub 2012 Jul 5.

DOI:10.1007/s00592-012-0412-3
PMID:22763581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3634985/
Abstract

Diabetes is associated with a greatly increased risk of cardiovascular disease (CVD), which cannot be explained only by known risk factors, such as smoking, hypertension, and atherogenic dyslipidemia, so other factors, such as advanced glycation end-products (AGEs) and oxidative stress, may be involved. In this frame, hyperglycemia and an increased oxidative stress (AGE formation, increased polyol and hexosamine pathway flux, and protein kinase C activation) lead to tissue damage, thus contributing to the onset of cardiovascular complications. Several studies have identified in various cell systems, such as monocytes/macrophages and endothelial cells, specific cellular receptors (RAGE) that bind AGE proteins. The binding of AGEs on RAGE induces the production of cytokines and intracellular oxidative stress, thus leading to vascular damage. Soluble RAGE levels have been identified as hypothetical markers of CVD, but, in this regard, there are sparse and conflicting data in the literature. The purpose of this review was to examine all the available information on this issue with a view to clarifying or at least highlighting the points that are still weak, especially from the point of clinical view.

摘要

糖尿病与心血管疾病(CVD)的风险大大增加有关,但这不能仅用已知的风险因素(如吸烟、高血压和致动脉粥样硬化性血脂异常)来解释,因此可能涉及其他因素,如糖基化终产物(AGEs)和氧化应激。在这种情况下,高血糖和氧化应激增加(AGE 形成、多元醇和己糖胺途径通量增加以及蛋白激酶 C 激活)导致组织损伤,从而导致心血管并发症的发生。多项研究已经在单核细胞/巨噬细胞和内皮细胞等各种细胞系统中鉴定出特定的细胞受体(RAGE),这些受体可以与 AGE 蛋白结合。AGE 与 RAGE 的结合会诱导细胞因子的产生和细胞内氧化应激,从而导致血管损伤。可溶性 RAGE 水平已被确定为 CVD 的假设标志物,但在这方面,文献中存在的数据很少且相互矛盾。本综述的目的是检查关于这个问题的所有可用信息,以便澄清或至少突出仍然薄弱的方面,特别是从临床角度来看。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e4/3634985/618cdf66f488/592_2012_412_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e4/3634985/c7cbcb3ea5ca/592_2012_412_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e4/3634985/618cdf66f488/592_2012_412_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e4/3634985/c7cbcb3ea5ca/592_2012_412_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e4/3634985/618cdf66f488/592_2012_412_Fig2_HTML.jpg

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