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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:通过脱敏中性粒细胞激活升级一氧化氮氧化胞胎素升级血液炎症中血液炎症的益处:编辑:“一氧化氮给予阿托伐他汀在血管炎症期间衰减中性粒细胞募集,与血浆胆固醇的变化相比,r.baettta等人。

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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中发病率和死亡率的主要原因。 临床表现,如心肌梗死和中风,主要依赖于动脉粥样硬化的发展和进展,这就是鉴定有前途的治疗靶点,需要详细了解其病理生理学和潜在的细胞和分子机制[1,2]。 动脉粥样硬化被广泛被认为是动脉壁的慢性炎症疾病[1,2]。 最初被多方刻录的参数促进,例如改性的低密度脂蛋白(LDL)或改变的流动,其特征在于内皮功能障碍。 内皮细胞的激活随后发动级联的自我放大炎性过程,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活化,粘附,逮捕和迁移[3]。

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