Methylglyoxal and glyoxalase I in atherosclerosis

Nordin M. J. Hanssen, Coen D. A. Stehouwer, Casper G. Schalkwijk*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

34 Citations (Web of Science)

Abstract

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, 6101 and AGEs in the context of plaque phenotype are discussed.
Original languageEnglish
Pages (from-to)443-449
JournalBiochemical Society Transactions
Volume42
DOIs
Publication statusPublished - Apr 2014

Keywords

  • advanced glycation end-product (AGE)
  • atherosclerosis
  • glyoxalase I
  • methylglyoxal
  • plaque rupture

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