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动脉样硬化中的易受伤害的斑块:专注于血管生成相关的表型交叉

Xin-Zheng Hou¹, Ying-Tian Yang¹, Jian-Ming Yao²

¹Department of Cardiovascular Diseases, Guang 'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

Frontiers in pharmacology

|January 29, 2026

概括

动脉样硬化 (AS) 斑块破裂,心脏病发作和中风的原因,与新血管化有关. 向血管内皮生长因子 (VEGF) 途径可能会稳定斑块,但需要安全的药物用于临床使用.

科学领域:

心血管研究研究心血管研究
病理学病理学病理学
血管新生研究研究

背景情况:

动脉样硬化 (AS) 是心血管疾病的主要原因,易受损伤的斑块破裂会引发心肌梗塞和中风等严重事件.
易受伤害的斑块通过血管性通路呈现出增加的新血管化,这矛盾地使斑块不稳定,尽管缓解了局部缺氧.

研究的目的:

审查血管新生和动脉样硬化中脆弱斑块形成的机制.
探索血管新生和AS过程之间的表型交叉.
为开发针对AS管理的血管内皮生长因子 (VEGF) 途径的新型治疗策略提供见解.

主要方法:

关于动脉样硬化,血管生成和VEGF信号的临床前和临床研究的文献综述.
分析新血管化和斑块不稳定机制之间的相互作用.
综合目前对针对VEGF途径的治疗策略的理解.

主要成果:

受VEGF通路调节的易受损伤的斑块中的新血管化有助于斑块的不稳定.
血管新生与细胞亡,细胞外矩阵重塑,炎症和氧化应激相互作用,产生反循环,使AS恶化.
向VEGF途径显示了增强斑块稳定性的临床前前期承诺.

结论:

了解血管新生和AS病原体之间的复杂关系对于开发有效的治疗方法至关重要.
在AS治疗中,VEGF途径是治疗干预的关键目标.
开发针对VEGF的安全可靠的药剂对于AS管理中的临床转化至关重要.

关键词:

血管新生是因为血管新生.灭症 (apoptosis) 是一种死亡的过程.动脉样硬化动脉样硬化细胞外矩阵是细胞外矩阵.这是一种炎症炎症炎症炎症.氧化应激是一种氧化应激.易受伤害的斑块是易受伤害的

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