血液氧化酶1决定了动脉样硬化病变的进展到一个易受损伤的斑块
Caroline Cheng1, Annemarie M Noordeloos, Viktoria Jeney
1Molecular Cardiology Laboratory, Experimental Cardiology, Thoraxcenter, Erasmus University Medical Center Rotterdam, Rotterdam 3015 CE, The Netherlands.
Circulation
|June 3, 2009
概括
血液氧化酶1 (HO-1) 诱导稳定了动脉疾病中脆弱的斑块. 这项研究表明,HO-1减少了斑块的不稳定性,作为对动脉样硬化进展的保护性反应.
科学领域:
- 心血管生物学 心血管生物学
- 动脉样硬化研究 动脉样硬化研究
- 分子医学是分子医学.
背景情况:
- 导致动脉硬性斑块从稳定转变为脆弱的分子机制尚未完全理解.
- 血氧酶1 (HO-1) 和其代谢物因其在动脉生成中对氧化应激的保护作用而得到认可.
研究的目的:
- 调查血红素氧酶1 (HO-1) 在动脉疾病中的斑块不稳定性进展中的作用.
- 在脆弱斑块发育的小鼠模型中评估HO-1的功能.
主要方法:
- 分析了112名患有冠状动脉疾病的患者的脑膜切除活检,根据斑块脆弱性分层.
- HO-1表达与斑块特征,炎症标志物 (MMP-9,IL-8,IL-6) 和细胞组件的相关性.
- 利用一种小鼠模型 (apolipoprotein E-/-小鼠) 来研究HO-1诱导 (原) 和抑制 (原) 对易受损伤的斑块发育的影响.
主要成果:
- 在患者中,HO-1表达与脆弱的斑块特征如巨细胞和脂质积累有很强的相关性,与光滑肌肉细胞和原相反.
- 在小鼠中,HO-1在易受伤害的病变上调;它的诱导减少了核大小和脂质积累,同时增加了帽子厚度和光滑肌肉细胞.
- 抑制HO-1加剧了斑块的脆弱性,而通过原或腺病毒转导诱导HO-1显示出显著的斑块稳定.
结论:
- HO-1诱导有效地逆转斑块的进展,将脆弱的斑块转移到更稳定的表型.
- 这表明HO-1作为对动脉样硬化进展的补偿性动脉样保护机制.
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