Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A
Effective therapy of atherosclerotic complications in patients with chronic kidney disease (CKD) is an unmet clinical need. Cardiovascular events are the most common cause of death. At a glomerular filtration rate <= 60 ml/min, these events are increased also after correction for common risk factors. Previous studies have reported enhanced vascular inflammation in mice and recently also in humans. Our current data show, in a mouse model of atherosclerosis in moderate renal impairment, that interleukin-17 receptor A is instrumental in this condition, and blockade of this pathway can normalize arterial inflammation even in advanced atherosclerosis. (C) 2018 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.
基金:
Deutsche Forschungsgemeinschaft; Else Kroner Fresenius Stiftung
第一作者单位:[1]Hannover Med Sch, Dept Internal Med, Div Nephrol & Hypertens, Hannover, Germany
通讯作者:
通讯机构:[1]Hannover Med Sch, Dept Internal Med, Div Nephrol & Hypertens, Hannover, Germany[*1]Hannover Med Sch, Dept Nephrol & Hypertens, OE 6840,Carl Neuberg Str 1, D-30625 Hannover, Germany
推荐引用方式(GB/T 7714):
Nordlohne Johannes,Helmke Alexandra,Ge Shuwang,et al.Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A[J].JACC-BASIC TO TRANSLATIONAL SCIENCE.2018,3(1):54-66.doi:10.1016/j.jacbts.2017.08.005.
APA:
Nordlohne, Johannes,Helmke, Alexandra,Ge, Shuwang,Rong, Song,Chen, Rongjun...&von Vietinghoff, Sibylle.(2018).Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A.JACC-BASIC TO TRANSLATIONAL SCIENCE,3,(1)
MLA:
Nordlohne, Johannes,et al."Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A".JACC-BASIC TO TRANSLATIONAL SCIENCE 3..1(2018):54-66