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Cellular and molecular mechanisms of statins: an update on pleiotropic effects

机译:他汀类药物和分子机制:脂肪效应的更新

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摘要

Coronary artery disease ( CAD) is the leading cause of death worldwide. The efficacy and safety of statins (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors) in primary and secondary prevention of CAD are confirmed in several large studies. It is well known that statins have some pleiotropic, anti-atherosclerotic effects. We review the molecular mechanisms underlying the beneficial effects of statins revealed in recently published studies. Endothelial cell injury is regarded as the classic stimulus for the development of atherosclerotic lesions. In addition, the inflammatory process plays an important role in the aetiology of atherosclerosis. In particular, chronic inflammation plays a key role in coronary artery plaque instability and subsequent occlusive thrombosis. Our previous reports and others have demonstrated beneficial effects of statins on endothelial dysfunction and chronic inflammation in CAD. A better understanding of the molecular mechanism underlying the effectiveness of statins against atherosclerosis may provide a novel therapeutic agent for the treatment of coronary atherosclerosis. The present review summarizes the cellular and molecular mechanism of statins against coronary atherosclerosis.
机译:冠状动脉疾病(CAD)是全世界死亡的主要原因。在几种大型研究中证实了他汀类药物(3-羟基-3-甲基戊族 - 辅酶抑制剂)中的疗效和安全性和二级预防CAD。众所周知,他汀类药物具有一些抗嗜血性抗动脉粥样硬化作用。我们审查了他汀类药物在最近公布的研究中显示的有益效果的分子机制。内皮细胞损伤被视为动脉粥样硬化病变的发展的经典刺激。此外,炎症过程在动脉粥样硬化的疾病中起着重要作用。特别是,慢性炎症在冠状动脉斑块不稳定性和随后的闭塞性血栓形成中起着关键作用。我们以前的报告和其他人已经证明了他汀类药物对CAD中内皮功能障碍和慢性炎症的有益作用。更好地理解依据对动脉粥样硬化的特定有效性的分子机制可提供一种用于治疗冠状动脉粥样硬化的新疗效。本综述总结了他汀类药物对冠状动脉粥样硬化的细胞和分子机制。

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