Hanssen Nordin M J, Stehouwer Coen D A, Schalkwijk Casper G
*Department of Internal Medicine, CARIM School for Cardiovascular Diseases, Maastricht University Medical Centre, Debeyelaan 25, 6202 AZ Maastricht, The Netherlands.
Biochem Soc Trans. 2014 Apr;42(2):443-9. doi: 10.1042/BST20140001.
Cardiovascular disease, caused predominantly by atherosclerotic plaque rupture, remains one of the leading causes of death. However, the mechanism of plaque rupture remains largely unknown. Recent studies have linked high metabolic activity in inflamed atherosclerotic plaques to the development of plaque rupture. AGEs (advanced glycation end-products) are known to be formed as a result of high metabolic activity and are higher in rupture-prone than stable plaques. Furthermore, AGEs seem to be more than mere markers of metabolic activity, as recent studies have elucidated that AGEs and their major precursor, MG (methylglyoxal), may have an important role in the progression of atherosclerosis and plaque rupture. MG can be detoxified by Glo1 (glyoxalase I), thereby preventing the accumulation of MG and MG-derived AGEs. In the present review, data concerning MG, Glo1 and AGEs in the context of plaque phenotype are discussed.
主要由动脉粥样硬化斑块破裂引起的心血管疾病仍然是主要死因之一。然而，斑块破裂的机制在很大程度上仍然未知。最近的研究将炎症性动脉粥样硬化斑块中的高代谢活性与斑块破裂的发生联系起来。晚期糖基化终产物（AGEs）已知是高代谢活性的结果，在易破裂斑块中比稳定斑块中含量更高。此外，AGEs似乎不仅仅是代谢活性的标志物，因为最近的研究表明AGEs及其主要前体甲基乙二醛（MG）可能在动脉粥样硬化进展和斑块破裂中起重要作用。MG可被乙二醛酶1（Glo1）解毒，从而防止MG和MG衍生的AGEs积累。在本综述中，讨论了与斑块表型相关的关于MG、Glo1和AGEs的数据。
