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首页> 外文期刊>Current opinion in lipidology >Statin therapy and angiogenesis.
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Statin therapy and angiogenesis.

机译：他汀类药物治疗和血管生成。

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SUMMARY: PURPOSE OF REVIEW Clinical studies suggested that 3-hydroxyl-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy has an additional cardiovascular protective activity that may function independently of the ability of statins to lower serum cholesterol. This paper reviews the available data on these effects and discusses the potential intracellular mechanisms involved.RECENT FINDINGS Experimental studies have clearly shown that statins protect against ischaemia-reperfusion injury of the heart, and exert pro-angiogenic effects by stimulating the growth of new blood vessels in ischaemic limbs of normocholesterolemic animals. The mechanisms underlying these serum lipid-independent statin effects are not completely understood, but there is increasing evidence that statins improve endothelial function through molecular mechanisms that mediate an increase in endothelium-derived nitric oxide. Recent research has revealed a link between statins and the serine/threonine protein kinase Akt that regulates multiple angiogenic processes in endothelial cells. In contrast to these data, it has also been reported that higher doses of statins can inhibit endothelial cell migration and angiogenesis.SUMMARY Statins have biphasic potential either to promote or inhibit angiogenesis. Low statin doses induce a pro-angiogenic effect through Akt activation and increase nitric oxide production, whereas high statin doses may decrease protein prenylation and inhibit cell growth. Notwithstanding, the clinical relevance of these serum lipid-independent effects is not fully understood. Further studies on the actions of statins on endothelial cells may lead to the identification of new pharmacological targets for the control of angiogenesis.
机译：概述：审查的目的临床研究表明3-羟基-3-甲基戊二酰辅酶A还原酶抑制剂（他汀类药物）疗法具有额外的心血管保护活性，其作用可能与他汀类药物降低血清胆固醇的能力无关。本文对这些作用的可用数据进行了综述，并讨论了潜在的细胞内机制。最近的研究表明，他汀类药物可预防心肌缺血再灌注损伤，并通过刺激新血管的生长发挥促血管生成作用。在常胆固醇动物的缺血肢体中。这些血清脂质​​依赖性他汀类药物作用的潜在机制尚不完全清楚，但是越来越多的证据表明他汀类药物通过介导内皮源性一氧化氮增加的分子机制改善了内皮功能。最近的研究表明，他汀类药物与丝氨酸/苏氨酸蛋白激酶Akt之间存在联系，后者可调节内皮细胞的多个血管生成过程。与这些数据相反，也有报道说，更高剂量的他汀类药物可以抑制内皮细胞迁移和血管生成。摘要他汀类药物具有促进或抑制血管生成的双相潜力。低剂量的他汀类药物通过Akt激活诱导促血管生成作用，并增加一氧化氮的产生，而高剂量的他汀类药物则可以减少蛋白质的异戊二烯化并抑制细胞生长。尽管如此，尚未完全了解这些血清脂质​​非依赖性作用的临床相关性。他汀类药物对内皮细胞作用的进一步研究可能会导致确定新的用于控制血管生成的药理学靶标。

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