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

机译:他汀类药物的细胞和分子机制:多效性效应的最新进展

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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)是全球主要的死亡原因。在几项大型研究中,他汀类药物(3-羟基-3-甲基戊二酰辅酶A还原酶抑制剂)在CAD的一级和二级预防中的有效性和安全性得到了证实。众所周知他汀类药物具有多效性,抗动脉粥样硬化作用。我们审查了在最近发表的研究中揭示的他汀类药物的有益作用的分子机制。内皮细胞损伤被认为是动脉粥样硬化病变发展的经典刺激。另外,炎症过程在动脉粥样硬化的病因中起重要作用。特别地,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关键作用。我们以前的报告和其他报告已证明他汀类药物对冠状动脉内皮功能障碍和慢性炎症的有益作用。他汀类药物抗动脉粥样硬化功效的分子机制的更好理解可能会为冠状动脉粥样硬化的治疗提供一种新型治疗剂。本综述总结了他汀类药物抗冠状动脉粥样硬化的细胞和分子机制。

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