A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage.

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作者： Allison E,Norlander ^[1] ; Mohamed A,Saleh ^[2] ; Arvind K,Pandey ^[3] ; Hana A,Itani ^[4] ; Jing,Wu ^[2] ; Liang,Xiao ^[1] ; Jooeun,Kang ^[2] ; Bethany L,Dale ^[1] ; Slavina B,Goleva ^[1] ; Fanny,Laroumanie ^[1] ; Liping,Du ^[2] ; David G,Harrison ^[5] ; Meena S,Madhur ^[1]

作者单位： Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA. ^[1] Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA. ^[2] Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt. ^[3] Division of Cardiology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA. ^[4] Vanderbilt Center for Quantitative Sciences, Vanderbilt University School of Medicine, Nashville, Tennessee, USA. ^[5]

关键词 Adaptive immunity Cardiology Cardiovascular disease Hypertension Inflammation

DOI 10.1172/jci.insight.92801

PMID 28679951

发布时间 2019-11-20

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2017年2卷13期

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A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage.

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A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage.

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