Transcriptomic Insights into the Anti-Inflammatory Effects of Curcuma longa in Diabetic Endothelial Dysfunction

Endothelial dysfunction is a central mechanism underlying vascular complications in diabetes mellitus and is closely associated with chronic inflammation, oxidative stress, and metabolic dysregulation. Curcuma longa (curcumin) has been widely investigated for its anti-inflammatory and antioxidant effects; however, its molecular actions on diabetic endothelium are not yet fully understood. Recent advances in transcriptomic technologies, including RNA sequencing and single-cell RNA sequencing, have provided novel insights into the endothelial signaling pathways regulated by curcumin. Emerging evidence indicates that curcumin modulates not only classical inflammatory pathways such as nuclear factor kappa B signaling, but also gene networks involved in endothelial glycocalyx integrity, oxidative stress responses, advanced glycation end product–receptor for advanced glycation end product signaling, and epigenetic regulation. Transcriptomic analyses further suggest that curcumin influences non-coding RNA pathways and redox-inflammatory crosstalk through coordinated regulation of antioxidant and immune-related genes. Additionally, single-cell transcriptomics highlights the potential heterogeneity of endothelial responses across different vascular beds. Despite promising findings, limitations including small sample sizes, poor bioavailability, and lack of standardized dosing protocols remain important challenges. Overall, transcriptomic evidence supports the concept of curcumin as a multi-target modulator of diabetic endothelial inflammation and suggests its potential role as an adjunctive therapeutic strategy in diabetes-related vascular disease.