内皮细胞特异性分子-1 (ESM1):在静脉血栓症中是一种内源性抗凝剂和保护因素
Changsheng Chen1, Xiaojuan Ge1, Dongxu Fu1
1School of Life Sciences, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
|January 10, 2026
概括
内皮细胞特异性分子-1 (ESM1) 作为一种新型抗凝剂,通过激活肝素辅因子II (HCII) 来减少静脉血栓形成. 静脉血栓栓塞 (VTE) 患者的ESM1水平升高表明其具有诊断和治疗潜力.
科学领域:
- 血管生物学 血管生物学
- 血液静止和血栓形成
- 蛋白质甘氨酸生物化学 蛋白质甘氨酸生物化学
背景情况:
- 自然抗凝机制的缺陷增加了血管封闭和血栓形成的风险.
- 内皮细胞特异性分子-1 (ESM1),一种蛋白质糖,在静脉血栓塞栓症 (VTE) 患者中发现度较高,但其在凝血中的作用尚不清楚.
研究的目的:
- 研究ESM1在调节凝血中的作用及其作为VTE诊断标记物和治疗点的潜力.
- 阐明ESM1抗凝剂活性背后的机制.
主要方法:
- 血清ESM1度测量在有和没有VTE的个体.
- 在斑马鱼和小鼠模型中,ESM1的抗凝潜力通过时间到遮 (TTO) 试验进行了评估.
- 在体外分析中研究了ESM1与内源性血栓激素抑制剂的相互作用,特别是肝素辅因子II (HCII).
主要成果:
- 与健康对照人群相比,VTE患者的血清ESM1水平明显高于健康对照人群,与D-dimer结合时改善了诊断歧视.
- 斑马鱼中ESM1的丧失导致了血管封闭,而ESM1的过度表达减少了静脉血栓形成.
- 通过ESM1淘汰的小鼠表现出改变的凝血,而这种变化在人类ESM1中被逆转. ESM1的抗凝功能取决于其激活HCII的葡萄糖氨基甘油 (GAG).
结论:
- 通过激活肝素辅因子II (HCII) 的介导,ESM1具有显著的抗凝性质.
- ESM1作为一种新型内源性抗凝剂和VTE的潜在生物标志物.
- 针对ESM1是一个有前途的治疗策略,可以预防静脉血栓形成.
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