Molecular mechanisms of methylglyoxal-induced aortic endothelial dysfunction in human vascular endothelial cells.

ABSTRACT: Methylglyoxal (MGO)-induced cellular apoptosis, oxidative stress, inflammation, and AGE formation are specific events that induce vascular endothelial cell (EC) toxicity in endothelial dysfunction (ED). MGO accumulates quickly in various tissues and plays a prominent role in the pathogeneses of several diabetic complications. Unbalanced angiogenesis is a gateway to the development of diabetic complications. EC apoptosis and autophagy work together to regulate angiogenesis by interacting with different angiogenic factors. In addition to understanding the deep mechanism regarding MGO-dependent autophagy/apoptosis may provide new therapeutic applications to treat diabetes and diabetic complications. Therefore, the present study aimed to investigate the regulatory effects of MGO-induced autoph

SUBMITTER: Lee JH 

PROVIDER: S-EPMC7256048 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature