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.
Conference Article| March 20 2014
Methylglyoxal and glyoxalase I in atherosclerosis
Nordin M.J. Hanssen;
Coen D.A. Stehouwer;
Casper G. Schalkwijk
Casper G. Schalkwijk 1
*Department of Internal Medicine, CARIM School for Cardiovascular Diseases, Maastricht University Medical Centre, Debeyelaan 25, 6202 AZ Maastricht, The Netherlands
1To whom correspondence should be addressed (emailC.Schalkwijk@maastricht-university.nl).
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Nordin M.J. Hanssen, Coen D.A. Stehouwer, Casper G. Schalkwijk; Methylglyoxal and glyoxalase I in atherosclerosis. Biochem Soc Trans 1 April 2014; 42 (2): 443–449. doi: https://doi.org/10.1042/BST20140001
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