BFGF alleviates diabetic endothelial dysfunction by downregulating Endoplasmic reticulum stress.

Abstract

Diabetes is a chronic metabolic disorder characterized by hyperglycemia, resulting from absolute or relative insufficiency in insulin secretion and disorder in insulin utilization. Diabetes has emerged as a global public health issue, with its incidence rate escalating year on year. Its vascular complications pose a severe challenge in clinical practice and constitute one of the principal causes of death among diabetes patients. Basic fibroblast growth factor, a member of the fibroblast growth factor family, exhibits a robust protective effect on numerous diseases. Consequently, it has become a research focus in the treatment of vascular complications related to diabetes. Nevertheless, the specific mechanism underlying basic fibroblast growth factor's vascular protective effect remains unclear. This study aims to explore whether basic fibroblast growth factor can alleviate endothelial dysfunction in diabetes by inhibiting endoplasmic reticulum stress. The research outcomes demonstrated that basic fibroblast growth factor significantly decreased the production of endoplasmic reticulum stress in db/db mice and endothelial cells incubated with high glucose and palmitic acid, augmented nitric oxide production, and reduced endothelial cell apoptosis. Treatment with the endoplasmic reticulum stress inducer Tunicamycin nullified the basic fibroblast growth factor mediated reduction in endoplasmic reticulum stress generation and endothelial protective effects. In conclusion, these discoveries imply that the endothelial protective effect of basic fibroblast growth factor in diabetes can be partially ascribed to its inhibition of endoplasmic reticulum stress.