Li Zhiru, Zeng Li, Huang Wei, Zhang Xinxing, Zhang Li, Xie Qin
Clinical Medical School, University of Electronic Science and Technology of China, Chengdu 610072, China.
Department of Geriatric Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
Biomedicines. 2025 May 9;13(5):1154. doi: 10.3390/biomedicines13051154.
Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is characterized by chronic intestinal inflammation and impaired epithelial barrier function. Emerging evidence highlights the critical role of vascular remodeling and angiogenesis in IBD pathogenesis. This review explores the intricate relationship between blood vessels and the intestinal epithelial barrier, emphasizing how aberrant vascularization contributes to barrier dysfunction and disease progression. In IBD, excessive angiogenesis is driven by hypoxia, immune cell infiltration, and pro-inflammatory cytokines, further perpetuating inflammation and tissue damage. Key angiogenic factors, such as vascular endothelial growth factor (VEGF), angiopoietins, and platelet-derived growth factor (PDGF), are upregulated in IBD, promoting pathological vessel formation. These newly formed vessels are often immature and hyperpermeable, exacerbating leukocyte recruitment and inflammatory responses. Given the pivotal role of angiogenesis in IBD, anti-angiogenic therapies have emerged as a potential therapeutic strategy. Preclinical and clinical studies targeting VEGF and other angiogenic pathways have shown promise in reducing inflammation and promoting mucosal healing. This review summarizes current knowledge on vascular-epithelial interactions in IBD, the mechanisms driving pathological angiogenesis, and the therapeutic potential of anti-angiogenic approaches, providing insights for future research and treatment development.
炎症性肠病(IBD),包括克罗恩病和溃疡性结肠炎,其特征为慢性肠道炎症和上皮屏障功能受损。新出现的证据凸显了血管重塑和血管生成在IBD发病机制中的关键作用。本综述探讨了血管与肠道上皮屏障之间的复杂关系,强调异常血管生成如何导致屏障功能障碍和疾病进展。在IBD中,缺氧、免疫细胞浸润和促炎细胞因子驱动过度血管生成,进一步使炎症和组织损伤持续存在。关键的血管生成因子,如血管内皮生长因子(VEGF)、血管生成素和血小板衍生生长因子(PDGF),在IBD中上调,促进病理性血管形成。这些新形成的血管通常不成熟且具有高通透性,加剧白细胞募集和炎症反应。鉴于血管生成在IBD中的关键作用,抗血管生成疗法已成为一种潜在的治疗策略。针对VEGF和其他血管生成途径的临床前和临床研究已显示出在减轻炎症和促进黏膜愈合方面的前景。本综述总结了目前关于IBD中血管 - 上皮相互作用、驱动病理性血管生成的机制以及抗血管生成方法的治疗潜力的知识,为未来的研究和治疗发展提供见解。