在人类动脉样硬化和静脉复缩中发生亡
J M Isner1, M Kearney, S Bortman
1Department of Medicine (Cardiology), St. Elizabeth's Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA.
Circulation
|June 1, 1995
概括
细胞亡,编程细胞死亡,存在于人类动脉样硬化和静脉复缩. 这一发现表明,亡有助于调节血管阻塞性病变中的细胞数量,特别是那些增殖率高的病变.
科学领域:
- 心血管生物学 心血管生物学
- 细胞病理学细胞病理学
- 血管医学 血管医学
背景情况:
- 细胞亡 (编程细胞死亡) 对于维持生殖组织中细胞数量的稳定至关重要.
- 之前的小鼠研究表明,亡减轻了在受伤动脉中的光滑肌肉细胞积累.
- 在人类血管病理学中亡的存在和程度仍然未确立.
研究的目的:
- 调查人类动脉样和静脉样样中亡的发生情况.
- 为了确定细胞亡是否在原发性动脉样硬化病变和静止性病变之间有所不同.
主要方法:
- 对接受切除术的患者的56个动脉样本进行免疫组织化学分析.
- 标本被分为主要动脉样硬化病变和静脉缩病变.
- 在每个样本中量化细胞的数量.
主要成果:
- 在63% (35/56) 的研究标本中检测到了亡.
- 与初级动脉样硬化病变相比 (43%的外周病变,29%的冠状动脉病变),静脉样病变显示出明显更高的亡频率 (93%的外周病变,86%的冠状动脉病变).
- 当存在时,亡通常涉及不到2%的细胞.
结论:
- 亡是人类血管病理的一个特征,包括静脉缩和动脉样硬化.
- 亡似乎在调节人类血管阻塞性病变的细胞性方面发挥着作用.
- 亡的程度可能与这些病变中的增殖活动有关.
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