ENDOCAN AS A BIOCHEMICAL MODULATOR OF INFLAMMATION, OXIDATIVE STRESS, CARDIAC REMODELING, AND TUMOR-RELATES SIGNALING

Endocan (endothelial cell-specific molecule-1, ESM1) has emerged as a pivotal proteoglycan involved in the biochemical regulation of inflammation, angiogenesis, and tumor progression. Our studies explored its role across different cellular contexts, highlighting its capacity to integrate cytokine-driven responses, oxidative stress, and oncogenic signaling pathways. In human chondrocytes, endocan expression was strongly induced by interleukin-1β (IL-1β), positioning it as a novel inflammatory marker.Functional experiments revealed that endocan knockdown attenuated IL-1β-mediated upregulation of angiogenesis-associated genes, suggesting its contribution to pathological neoangiogenesis in joint diseases1. In lung cancer cells, endocan promoted pro-tumorigenic phenotypes, including enhanced proliferation and migration, while regulating the expression of oncogenic long non-coding RNAs (lncRNAs) H19 and HULC 2. In cardiac fibroblasts, endocan acted as a biochemical integrator of TGF-β/Smad and AKT/ERK signaling with lncRNA modulation, supporting its role in fibrotic remodeling. Finally, under oxidative stress conditions, NRF2 was shown to modulate endocan expression, linking redox homeostasis to endocan-dependent pathways. Collectively, these findings identify endocan as a biochemical hub orchestrating multiple signaling cascades across inflammatory, oxidative, and tumorigenic contexts. Targeting endocan or its downstream effectors may thus provide novel therapeutic strategies in inflammatory disorders, cancer, and cardiovascular disease