GSE109441
RNA-seq of a high glucose induced oxidative stress and apoptosis model on primary rat cardiomyocytes
Diabetic hyperglycemia promotes reactive oxygen species (ROS) production to lead to oxidative stress and apoptosis responsible for progressive deterioration of the structure and function of organs. It has been indicated that factors and pathways regulating ROS production and the cellular redox state play a key role in the progression of diabetes and diabetes complications including cardiomyopathy. Recent studies had demonstrated that long non-coding RNAs (lncRNAs) played crucial roles on modulation of oxidative stress and apoptosis activity. In this study, we first established a high glucose induced oxidative stress and apoptosis model on primary rat cardiomyocytes. ROS formation and apoptosis activity were significantly increased at 24h/48h after high glucose stimulation. RNA sequencing analysis was applied to detect differentially expressed lncRNAs during cardiomyocytes oxidative stress and apoptosis. Overall design: RNA-seq of a high glucose induced oxidative stress and apoptosis model on primary rat cardiomyocytes and control groups at 24h/48h.