Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A

摘要

class="kwd-title">Key Words: atherosclerosis, chronic kidney disease, interleukin 17, macrophage class="kwd-title">Abbreviations and Acronyms: CKD, chronic kidney disease; IL, interleukin; Il17ra, interleukin-17 receptor A (gene name); LDLr, low-density lipoprotein receptor; PCR, polymerase chain reaction class="head no_bottom_margin" id="abs0010title">SummaryEffective 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.