Diabetic complications, which are grave sequelae of diabetes, are the primary cause of mortality among diabetic individuals. Effective prevention and management of these complications are essential for reducing mortality rates. Controlling blood glucose levels is a fundamental aspect of treatment, yet it is fraught with challenges. The etiology of diabetic complications is multifactorial, encompassing hyperglycemia, inflammation, and endothelial cell dysfunction. Ferroptosis, a novel form of regulated cell death characterized by heightened lipid peroxidation and reactive oxygen species (ROS) accumulation, has been implicated in endothelial cell injury and dysfunction. Inhibition of ferroptosis has been shown to mitigate endothelial cell dysfunction, suggesting its potential as a therapeutic target for diabetic complications. This article comprehensively reviews the mechanism of ferroptosis, the targeting regulation of endothelial cells, the interaction between endothelial cells and parenchymal cells, and the relationship between diabetes complications and endothelial cell injury. Through an in-depth examination of the nexus between endothelial ferroptosis and diabetic complications, we aim to offer innovative insights and perspectives for advancing treatment strategies.
Xie et al. (Tue,) studied this question.