Diabetes is a well-known risk factor for the development of cardiovascular diseases. Diabetes affects cardiac tissue through several different, yet interconnected, pathways. Damage to endothelial cells from direct exposure to high blood glucose is a primary cause of deregulated heart function. Toxic by-products of non-enzymatic glycolysis, mainly methylglyoxal, have been shown to contribute to the endothelial cell damage. Methylglyoxal is a precursor for advanced glycation end-products, and, although it is detoxified by the glyoxalase system, this protection mechanism fails in diabetes. Recent work has identified methylglyoxal as a therapeutic target for the prevention of cardiovascular complications in diabetes. A better understanding of the glyoxalase system and the effects of methylglyoxal may lead to more advanced strategies for treating cardiovascular complications associated with diabetes.
- cardiovascular disease
- endothelial dysfunction
Glyoxalase Centennial: 100 Years of Glyoxalase Research and Emergence of Dicarbonyl Stress: A Biochemical Society Focused Meeting held at the University of Warwick, U.K., 27–29 November 2013. Organized and Edited by Naila Rabbani and Paul Thornalley (University of Warwick, U.K.).
Abbreviations: AGE, advanced glycation end-product; EC, endothelial cell; ED, endothelial dysfunction; Glo, glyoxalase; ICAM, intercellular adhesion molecule; JNK, c-Jun N-terminal kinase; MG, methylglyoxal; NAC, N-acetylcysteine; NF-κB, nuclear factor κB; RAGE, receptor for AGEs; ROS, reactive oxygen species; STZ, streptozotocin; VCAM, vascular cell adhesion molecule
- © The Authors Journal compilation © 2014 Biochemical Society