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首页> Cardiovascular research> Endothelial and cardiomyocyte PI3Kβ divergently regulate cardiac remodelling in response to ischaemic injury.

Endothelial and cardiomyocyte PI3Kβ divergently regulate cardiac remodelling in response to ischaemic injury.

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作者： Xueyi,Chen ^[1] ; Pavel,Zhabyeyev ^[2] ; Abul K,Azad ^[1] ; Wang,Wang ^[2] ; Rachel A,Minerath ^[1] ; Jessica,DesAulniers ^[2] ; Chad E,Grueter ^[3] ; Allan G,Murray ^[4] ; Zamaneh,Kassiri ^[1] ; Bart,Vanhaesebroeck ^[2] ; Gavin Y,Oudit ^[4]

作者单位： Department of Medicine, University of Alberta, Edmonton, Alberta, Canada. ^[1] Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada. ^[2] Department of Physiology, University of Alberta, Edmonton, Alberta, Canada. ^[3] Division of Cardiovascular Medicine, Department of Internal Medicine, Francois M. Abboud Cardiovascular Research Center, Fraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA, USA. ^[4] University College London Cancer Institute, University College London, London, UK. ^[5]

关键词 Angiogenesis Cardiomyocyte death Myocardial infarction PI3Kβ Remodelling

主题词动物(Animals);细胞, 培养的(Cells, Cultured);I类磷脂酰肌醇3-激酶类(Class I Phosphatidylinositol 3-Kinases);疾病模型, 动物(Disease Models, Animal);内皮细胞(Endothelial Cells);人类(Humans);男(雄)性(Male);小鼠, 基因敲除(Mice, Knockout);心肌梗死(Myocardial Infarction);心肌再灌注损伤(Myocardial Reperfusion Injury);肌细胞, 心脏(Myocytes, Cardiac);新生血管化, 生理性(Neovascularization, Physiologic);一氧化氮合酶Ⅲ型(Nitric Oxide Synthase Type III);磷酰化(Phosphorylation);原癌基因蛋白质c-akt(Proto-Oncogene Proteins c-akt);信号传导(Signal Transduction);心室重构(Ventricular Remodeling)

DOI 10.1093/cvr/cvy298

PMID 30496354

发布时间 2024-02-07

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Cardiovascular research

Cardiovascular research

2019年115卷8期

1343-1356页

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