Potential for anti‑angiogenic therapy targeting the receptor for advanced glycation end products/VEGF axis in ulcerative colitis (Review)

Ulcerative colitis (UC), a major form of inflammatory bowel disease, has a global incidence of ~10.6 per 100,000 individuals. The long‑term side effects and dependency issues associated with conventional UC therapies have become increasingly evident, highlighting the need for more effective and safer treatment options. In previous years, clinical research on small‑molecule targeted drugs against UC has achieved notable progress; however, the underlying pathogenesis and therapeutic mechanisms of UC still require deeper investigation. The receptor for advanced glycation end products (RAGE) is a pattern recognition receptor that binds both pathogen‑associated molecular patterns and damage‑associated molecular patterns, thereby mediating inflammatory and cellular stress responses. Concurrently, vascular endothelial growth factor (VEGF), a key regulator of angiogenesis, is markedly upregulated in patients with UC and associates with disease severity. The RAGE/VEGF signaling axis has thus emerged as a notable target for antiangiogenic therapy in UC. Interventions aimed at disrupting the interaction between RAGE and its ligands, inhibiting RAGE pathway activation or suppressing VEGF upregulation have demonstrated promising potential to alleviate symptoms and slow disease progression. The present review summarizes previous advances in UC‑targeted therapeutics and elucidates the role of the RAGE/VEGF axis in UC pathophysiology, highlighting the potential mechanisms and clinical prospects of antiangiogenic strategies targeting this pathway.