位置：成果数据库 > 期刊 > 期刊详情页
Simvastatin Increases the Activity of Endothelial Nitric Oxide Synthase via Enhancing Phosphorylation
  • 时间：0
  • 分类：R44[医药卫生—诊断学;医药卫生—临床医学]
  • 作者机构：[1]The Institute of Hypertension and Department of lnternal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science, Wuhan 430030, China, [2]Davis Heart ＆ Lung Research Institute, the Ohio State University Medical Center, Ohio 43210, USA
  • 相关基金：This project was supported by grants from National Natural Sciences Foundation of China （No. 30430320 and 30770882） and National 973 Project （No. 2007CB512004）.
作者： 李小霞[1], 汪培华[1], 徐西振[1], 王勇[1], 夏永[2], 汪道文[1]
关键词： HMG-COA, 医学, 临床, 诊断, simvastatin, nitric oxide synthase, phosphorylation, endothelial cells
中文摘要：

Xiaoxia LI, E-mail： lxx35913@ 163.com.Xiaoxia LI and Peihua WANG contributed equally to this work. Corresponding author

同期刊论文项目
内质网应激通路激活介导的心肌损伤和心力衰竭及其干预研究
期刊论文 12
花生四烯酸细胞色素P450表氧化酶保护心血管系统、防止心血管疾病及其机理研究
期刊论文 10 会议论文 3
同项目期刊论文
Arachidonic Acid Epoxygenase Metabolites Stimulate Endothelial Cell Growth and Angiogenesis Involved
Regulation of Endothelial Nitric-oxide Synthase Activity through Phosphorylation in Response to Epox
Genetic variation in cytochrome P450 2J2 and soluble epoxide hydrolase and risk of ischemic stroke i
Cytochrome P450 epoxygenase promotes human cancer metastasis
Long-term modifications of blood pressure in normotensive and spontaneously hypertensive rats by gen
Cytochrome P450 2J2 promotes the neoplastic phenotype of carcinoma cells and is upregulated in human
Effects of epoxyeicosatrienoic acids on levels of eNOS phosphorylation and relevant signaling transd
Cytochrome P450 Epoxygenases Protect Endothelial Cells from Apoptosis Induced by Tumor Necrosis Fact
Throat Infection, Neck and Chest Pain and Cardiac Response： A Persistent Infection-Related Clinical Syndrome
Improvement of mechanical heart function by trimetazidine in db/db mice
The epoxyeicosatrienoic acid-stimulated phosphorylation of EGF-R involves the activation of metallop
Simvastatin Increases the Activity of Endothelial Nitric Oxide Synthase via Enhancing Phosphorylatio
β1-AR持久兴奋通过CaMKIIδ-内质网应激凋亡通路导致心力衰竭的机制
美托洛尔下调CaMKIIδC-p38通路对异丙肾上腺素诱导心力衰竭的保护机制