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首页> 外文期刊>Cardiovascular drugs and therapy >Nitric oxide-donating statins upgrade the benefits of lipid-lowering in vascular inflammation by desensitizing neutrophil activation: editorial to: 'Nitric oxide-donating atorvastatin attenuates neutrophil recruitment during vascular inflammation independent of changes in plasma cholesterol' by R. Baetta et al.
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Nitric oxide-donating statins upgrade the benefits of lipid-lowering in vascular inflammation by desensitizing neutrophil activation: editorial to: 'Nitric oxide-donating atorvastatin attenuates neutrophil recruitment during vascular inflammation independent of changes in plasma cholesterol' by R. Baetta et al.

机译:捐赠一氧化氮的他汀类药物通过使中性粒细胞激活不敏感来提高降低血管炎症的脂质的益处:社论:“捐赠一氧化氮的阿托伐他汀可在血管炎症期间减弱中性粒细胞的募集,而与血浆胆固醇的变化无关”。

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摘要

Cardiovascular events are the leading cause for morbidity and mortality in Western societies. Clinical manifestations such as myocardial infarction and stroke mainly rely on the development and progression of atherosclerosis, which, in terms of identifying promising therapeutic targets, requires detailed understanding of its pathophysiology and underlying cellular as well as molecular mechanisms [1,2]. Atherosclerosis has widely been accepted to be a chronic inflammatory disease of the arterial wall [1,2]. Initially promoted by multifaceted parameters such as modified low density lipoprotein (LDL) or altered flow, it is characterized by endothelial dysfunction. Activation of endothelial cells subsequently launches a cascade of self-amplifying inflammatory processes such as expression of chemokines, cytokines and adhesion molecules, all of which then contribute to leukocyte activation, adhesion, arrest and transmigration [3].
机译:心血管事件是西方社会发病率和死亡率的主要原因。心肌梗塞和中风等临床表现主要取决于动脉粥样硬化的发生和发展,就确定有希望的治疗靶点而言,需要详细了解其病理生理学和潜在的细胞以及分子机制[1,2]。动脉粥样硬化已被广泛接受为动脉壁的慢性炎性疾病[1,2]。最初是由诸如修饰的低密度脂蛋白(LDL)或流量改变等多方面参数促进的,其特征在于内皮功能障碍。内皮细胞的激活随后启动了一系列自放大的炎症过程,例如趋化因子,细胞因子和粘附分子的表达,所有这些都有助于白细胞的活化,粘附,阻滞和迁移[3]。

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