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Although cellular senescence initially functions as a tumor\u2010suppressive barrier, the persistent accumulation of senescent cells can promote disease progression through the senescence\u2010associated secretory phenotype (SASP). Key SASP mediators, including VEGF, IL\u20108\/CXCL8, and matrix metalloproteinases (MMPs), reprogram endothelial and stromal compartments, driving aberrant neovascularization, vascular leakiness, extracellular\u2010matrix remodeling, and tissue hypoxia that further reinforce inflammation and genomic instability. Emerging evidence also highlights marked heterogeneity among senescent epithelial, stromal, endothelial, and immune\u2010cell populations within the inflamed intestinal mucosa, suggesting that distinct senescent subsets may differentially shape angiogenesis and malignant transformation. This review synthesizes current evidence linking inflammation\u2010induced senescence to vascular dysfunction and the transition from IBD to colitis\u2010associated colorectal cancer, and discusses therapeutic opportunities targeting the senescence\u2013angiogenesis axis. By clarifying how the aging microenvironment reshapes intestinal angiogenesis, we propose a mechanistic framework for early intervention and cancer prevention in colitis\u2010associated neoplasia.<\/jats:p>","DOI":"10.1111\/acel.70570","type":"journal-article","created":{"date-parts":[[2026,6,15]],"date-time":"2026-06-15T05:01:54Z","timestamp":1781499714000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["The Aging Microenvironment Shapes Angiogenic Remodeling in\n                    <scp>IBD<\/scp>\n                    \u2010Associated Colorectal Carcinogenesis"],"prefix":"10.1111","volume":"25","author":[{"given":"Ruoshu","family":"Duan","sequence":"first","affiliation":[{"name":"Department of Gastroenterology The Second Affiliated Hospital and Yuying Children\u2019s Hospital of Wenzhou Medical University  Wenzhou Zhejiang P. R. 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