心肌原的循环在高伤性心肌病症中的转化
Raffaella Lombardi1, Sandro Betocchi, Maria Angela Losi
1Department of Clinical Medicine, Cardiovascular and Immunological Sciences, Federico II University School of Medicine, Naples, Italy.
Circulation
|September 4, 2003
概括
在高性心肌病 (HCM) 中,原蛋白的循环增加. 增强的I型原蛋白合成和抑制的矩阵金属蛋白酶 (MMPs) 有助于HCM患者的舒张功能障碍.
科学领域:
- 心血管研究研究心血管研究
- 细胞外基质的生物化学
- 心脏病理生理学 心脏病理生理学
背景情况:
- 心肌间歇性纤维化是心肌缩性心肌病 (HCM) 的一个标志.
- 了解原体重塑对于理解HCM进展至关重要.
研究的目的:
- 为了研究高性心肌病 (HCM) 患者的原循环标记物.
- 评估 HCM 中的原循环和左心室 (LV) 扩张功能之间的关系.
主要方法:
- 放射性免疫分析和ELISA用于测量原合成 (PIIINP,PICP,PINP),降解 (ICTP),矩阵金属蛋白酶 (MMP:MMP-1,MMP-2,MMP-9) 和金属蛋白酶-1 (TIMP-1) 的组织抑制剂.
- 心声学评估了左心室 (LV) 的透析功能,估计了使用传导 (A) 和肺静脉 (AR) 波长 (A-Ar) 的被动透析功能.
- 具有限制性或伪正常的LV填充模式的患者被确定为具有被动性扩张功能障碍.
主要成果:
- 与对照组相比,HCM患者的PIIINP,ICTP,MMP-2,MMP-9和总TIMP-1水平显著更高.
- PIIINP水平与LV终端-透气直径相反相关.
- 被动扩张功能 (A-Ar) 与原I积累标记物 (PICP,PINP,ICTP) 相反,与MMP-1和MMP-2水平直接相关.
结论:
- 在患有缩性心肌病 (HCM) 的患者中,原蛋白的循环量显著增加.
- 抑制MMP-1和MMP-2,加上流行的 I 原合成与降解相比,导致HCM中被动的透缩功能障碍.
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