BFGF alleviates diabetic endothelial dysfunction by downregulating Endoplasmic reticulum stress.

Area of Science:

• Endocrinology
• Vascular Biology
• Molecular Medicine

Background:

• Diabetes mellitus is a growing global health concern characterized by hyperglycemia.
• Diabetic vascular complications are a major cause of morbidity and mortality.
• Basic fibroblast growth factor (bFGF) shows promise for treating diabetic vascular complications, but its mechanism is unclear.

Purpose of the Study:

• To investigate if bFGF alleviates endothelial dysfunction in diabetes by inhibiting endoplasmic reticulum (ER) stress.
• To elucidate the role of ER stress in bFGF's protective effects on diabetic vasculature.

Main Methods:

• Utilized db/db mice and endothelial cells exposed to high glucose and palmitic acid.
• Assessed ER stress markers, nitric oxide (NO) production, and endothelial cell apoptosis.
• Investigated the effect of the ER stress inducer Tunicamycin on bFGF's protective actions.

Main Results:

• bFGF significantly reduced ER stress in diabetic mouse models and high-glucose/palmitic acid-treated endothelial cells.
• bFGF increased nitric oxide production and decreased endothelial cell apoptosis.
• Tunicamycin treatment abolished the beneficial effects of bFGF, indicating ER stress mediation.

Conclusions:

• bFGF exerts protective effects on diabetic endothelial cells partly by inhibiting endoplasmic reticulum stress.
• These findings suggest bFGF as a potential therapeutic agent for diabetic vascular complications via ER stress modulation.