与肥胖相关的循环内皮衍生细胞外微囊细胞和内皮纤维溶解功能障碍的肥胖相关升高
Samuel T Ruzzene1, Auburn R Berry1, Vinicius P Garcia1
1Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado Boulder, Boulder, Colorado, United States.
American journal of physiology. Heart and circulatory physiology
|December 18, 2025
概括
肥胖会损害内皮细胞释放组织类型等离子体激活剂 (t-PA) 的能力,增加血栓形成的风险. 肥胖症中循环内皮细胞衍生的微细胞 (EMV) 的升高与这种纤维溶解功能障碍有关,这表明EMV是潜在的生物标志物.
科学领域:
- 血管生物学和血栓形成
- 内皮质功能障碍 在内皮质功能障碍
- 肥胖病理生理学 肥胖病理生理学
背景情况:
- 肥胖与内皮功能受损和血栓形成风险增加有关.
- 由内皮细胞释放的组织类型等离子体激活剂 (t-PA) 对于纤维素分解至关重要.
- 循环内皮细胞衍生的微 (EMVs) 涉及血管疾病,在肥胖中升高.
研究的目的:
- 调查循环EMV与肥胖成年人的内皮纤维解质功能障碍之间的关联.
- 为了确定肥胖症中EMV的升高是否与降低的t-PA释放相关.
主要方法:
- 这项研究包括28名静坐的成年人 (14人体重正常,14人肥胖),年龄在45-71岁之间.
- 循环EMVs (CD144+) 使用流细胞计量量化.
- 在体内内皮质t-PA释放被测量为对布拉迪基宁 (BK) 和酸 (SNP) 输注的反应.
主要成果:
- 与正常体重的成年人相比,肥胖的成年人表现出~170%更高的循环EMV水平 (P < 0.001).
- 针对BCK的内皮t-PA释放在肥胖的成年人中明显较低 (~30%) (P = 0.007).
- 循环中的EMV与BK反应的峰值和总t-PA释放相反相关 (r = -0.67和r = -0.53,分别;P < 0.004).
结论:
- 肥胖成年人循环EMV的增加与内皮t-PA释放的减少有关.
- 循环的EMV可以作为与肥胖相关的内皮纤维溶解功能障碍的新型系统生物标志物.
- 这些发现强调EMV是肥胖个体血栓形成风险增加的潜在指标.
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