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Shinohara, M., Thornalley, P.J., Giardino, I., Beisswenger, P., Thorpe, S.R., Onorato, J., et al. (1998) Overexpression of Glyoxalase-I in Bovine Endothelial Cells Inhibits Intracellular Advanced Glycation Endproduct Formation and Prevents Hyperglycemia-Induced Increases in Macromolecular Endocytosis. Journal of Clinical Investigation, 101, 1142-1147.
https://doi.org/10.1172/jci119885

has been cited by the following article:

• TITLE: Molecular Regulators of Diabetic Endothelial Dysfunction

  AUTHORS: Neetu Sud

  KEYWORDS: Diabetes, Endothelial Dysfunction, Hyperglycemia, Oxidative Stress, Inflammation

  JOURNAL NAME: Journal of Diabetes Mellitus, Vol.16 No.2, May 28, 2026

  ABSTRACT: Diabetes is a highly prevalent disease worldwide. It is associated with perturbation in glucose metabolism. Diabetic environment has immense impact on endothelial cells (ECs) which line the endothelium and regulate many vascular functions. Hyperglycemia (HG) is a hallmark of diabetes and it promotes formation of Advanced Glycation End Products (AGEs), oxidative stress, mitochondrial abnormalities, inflammation, polyol pathway, hexosamine pathway, etc. These cellular processes hamper EC function resulting in endothelial cell dysfunction (ED). Several diabetic vascular complications are initiated by ED. The persistence of diabetes related endothelial cell damage even after normalization of glucose levels is known as metabolic memory, which further accelerates diabetic complications. Therefore, diabetes makes patients more susceptible to vascular complications. Herein, some important diabetes related cellular phenomena that perturb EC function are described briefly. Understanding these deleterious phenomena is essential for developing treatment strategies to ameliorate diabetic ED.