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动脉和大动脉的化被慢性病中的弹性甲素S缺乏消除了

Elena Aikawa¹, Masanori Aikawa, Peter Libby

¹Center for Molecular Imaging Research, Massachusetts General Hospital, Harvard Medical School, 149 13th St, Room 5420, Charlestown, MA 02129, USA. eaikawa@mgh.harvard.edu

|March 25, 2009

概括

甲素S (catS) 在慢性病 (CRD) 中驱动动动脉和大动脉结石化. 抑制catS可能会在CRD患者中预防心血管疾病进展.

科学领域:

心血管生物学心血管生物学
腎臟病學 (nephrology) 是一種醫學專業.
分子成像学分子成像学

背景情况:

50%的慢性病 (CRD) 患者死于心血管原因,通常是由于动脉和膜疾病.
在CRD中加速化的机制尚不清楚;目前的疗法无法阻止进展.
炎症和弹性质降解产物与心血管化有关.

研究的目的:

为了测试cathepsin S (catS) 在CRD的动脉样硬化小鼠中加速化的体内假设.
研究catS诱导的弹性溶解在心血管化中的作用.

主要方法:

使用了经过手术诱导的CRD (5/6腎切除术) 的转基因小鼠 (apoE(-/-) /catS(+/+) 和apoE(-/-) /catS(-/-).
使用分子成像剂可视化catS活动和骨质生成 in vivo.
进行定量组织学,以评估主动脉和主动脉中的弹性质碎片化和化.

主要成果:

在CRD小鼠中,血清酸盐,肌素和囊素C的水平升高.
在体内成像显示,缺乏catS删除的CRD小鼠中,catS和骨质生成活性增加.
带有catS删除的CRD小鼠显著减少了大动脉和膜化和弹性质碎片化.
实验室研究证实,catS和弹性质可以促进平滑肌肉细胞化.

结论:

甲素S (catS) 诱导的弹性溶解直接加速慢性病 (CRD) 中的动脉和大动脉结石化.
这项研究为CRD中心血管化的病理生理学提供了新的见解.
准catS可能为预防CRD患者心血管并发症提供治疗策略.

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