Vascular inflammation and cancer malignancy

IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE

Journal of Oral Biosciences Pub Date : 2025-05-20 DOI:10.1016/j.job.2025.100671

Yuya Sakurai , Li Yu , Aya Matsuda , Nako Maishi , Kyoko Hida

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Abstract

Background

Vascular inflammation is a key contributor to cancer progression and metastasis. Tumor endothelial cells (TECs) respond to microbial, metabolic, and therapeutic stimuli by upregulating adhesion molecules and cytokines, which facilitates tumor cell adhesion and immune evasion.

Highlight

This review focuses on three representative vascular inflammatory triggers: Streptococcus mutans-induced endothelial activation, the oxLDL/LOX-1 signaling axis, and chemotherapy-induced vascular dysfunction. These mechanisms converge to establish a pre-metastatic niche. Emerging strategies including microbiota modulation, metabolic targeting, and low-dose metronomic (LDM) chemotherapy, have shown promise in preclinical studies for preserving vascular integrity and reducing inflammation.

Conclusion

Targeting vascular inflammation is a novel therapeutic approach to suppressing metastasis and cardiovascular events. Further studies are required to validate predictive biomarkers and optimize these strategies for clinical applications.

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血管炎症和恶性肿瘤

背景：血管炎症是癌症进展和转移的关键因素。肿瘤内皮细胞（tec）通过上调粘附分子和细胞因子对微生物、代谢和治疗刺激做出反应，从而促进肿瘤细胞的粘附和免疫逃逸。本文综述了三种具有代表性的血管炎症触发因素：变形链球菌诱导的内皮激活、oxLDL/LOX-1信号轴和化疗诱导的血管功能障碍。这些机制共同建立了转移前生态位。包括微生物群调节、代谢靶向和低剂量节律化疗在内的新兴策略在临床前研究中显示出保持血管完整性和减少炎症的希望。结论靶向血管炎症是抑制血管转移和心血管事件的新途径。需要进一步的研究来验证预测性生物标志物并优化这些策略以用于临床应用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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