Tousoulis Dimitris, Antoniades Charalambos, Stefanadis Christodoulos
Int J Cardiol. 2008 Jan 11;123(2):91-3. doi: 10.1016/j.ijcard.2007.04.054. Epub 2007 Jun 13.
Endothelial nitric oxide synthase (eNOS), the main source of endothelium-derived nitric oxide (NO), appears to be a rational therapeutic target in atherosclerosis. The exact mechanisms regulating eNOS protein expression in human vasculature are still under intensive investigation. Recent evidence suggests that statin treatment induces the expression of eNOS in vascular endothelium, leading to a respective improvement of endothelial function. Among other mechanisms, it seems that statins increase eNOS protein levels in the vasculature, partly by up-regulating klotho protein expression. This novel observation is consistent with several lines of clinical evidence suggesting that statins have antiatherogenic effects in human vasculature, by mechanisms other than lipid-lowering.
内皮型一氧化氮合酶（eNOS）是内皮源性一氧化氮（NO）的主要来源，似乎是动脉粥样硬化合理的治疗靶点。调控人类血管中eNOS蛋白表达的确切机制仍在深入研究中。最近的证据表明，他汀类药物治疗可诱导血管内皮中eNOS的表达，从而相应改善内皮功能。在其他机制中，他汀类药物似乎部分通过上调klotho蛋白表达来增加血管中eNOS蛋白水平。这一新发现与多项临床证据一致，表明他汀类药物通过降脂以外的机制对人类血管具有抗动脉粥样硬化作用。
