思考在冠心病中 HDL 功能的差异。
PON-dering differences in HDL function in coronary artery disease.
机构信息
Division of Pulmonary and Vascular Biology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9063, USA.
出版信息
J Clin Invest. 2011 Jul;121(7):2545-8. doi: 10.1172/JCI57671. Epub 2011 Jun 23.
Abstract
HDL cholesterol activates endothelial cell production of the atheroprotective signaling molecule NO, and it promotes endothelial repair. In this issue of the JCI, Besler et al. provide new data indicating that HDL from stable coronary artery disease (CAD) or acute coronary syndrome patients inhibits rather than stimulates endothelial NO synthesis and endothelial repair. This may be related to decreased HDL-associated paraoxonase 1 (PON1) activity. These observations support the concept that the cardiovascular impact of HDL is not simply related to its abundance, and the translation of the present findings to prospective studies of CAD risk and to evaluations of HDL-targeted therapeutics is a logical future goal.
摘要
高密度脂蛋白胆固醇可激活内皮细胞产生具有抗动脉粥样硬化作用的信号分子一氧化氮，并促进内皮修复。在本期 JCI 中，Besler 等人提供了新的数据，表明来自稳定性冠状动脉疾病（CAD）或急性冠状动脉综合征患者的 HDL 抑制而非刺激内皮细胞一氧化氮合成和内皮修复。这可能与 HDL 相关的对氧磷酶 1（PON1）活性降低有关。这些观察结果支持这样一种概念，即 HDL 的心血管影响不仅仅与其丰度有关，将目前的发现转化为 CAD 风险的前瞻性研究以及对 HDL 靶向治疗的评估是一个合乎逻辑的未来目标。
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本文引用的文献
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