Low glucose induces mitochondrial reactive oxygen species via fatty acid oxidation in bovine aortic endothelial cells.

ABSTRACT:

Aims/introduction

Overproduction of reactive oxygen species (ROS) in endothelial cells (ECs) plays a pivotal role in endothelial dysfunction. Mitochondrial ROS (mtROS) is one of the key players in the pathogenesis of diabetic vascular complications. Hypoglycemia is linked to increased ROS production and vascular events; however, the underlying mechanisms remain unclear. In the present study, we aimed to determine whether and how low glucose (LG) mediates mtROS generation in ECs, and to examine the impact of LG-induced mtROS on endothelial dysfunction.

Materials and methods

Metabolomic profiling, cellular oxygen consumption rate, mtROS, endothelial nitric oxide synthase phosphorylation, and the expression of vascular cell adhesion molecule-1 or intercellular adhesion molecule

SUBMITTER: Kajihara N 

PROVIDER: S-EPMC5668512 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature