Targeting Complement Component 1q Ameliorates Diabetic Endothelial Inflammation Via Orphan Nuclear Receptor 4a1–Dependent Suppression of Nuclear Factor κB Signaling

Puntos clave

• To investigate the role of C1q in endothelial inflammation related to diabetes and explore its mechanism of action.
• Examined the effects of C1q downregulation on endothelial cells
• Analyzed the role of orphan nuclear receptor 4a1 in signaling pathways
• Investigated nuclear factor kappa b (NF-κB) activation in the context of diabetes
• C1q downregulation significantly reduced endothelial inflammation
• Orphan nuclear receptor 4a1 was crucial for suppression of NF-κB signaling
• Findings offer insights for potential therapeutic approaches against diabetic vascular complications