Inhibition of STAT3 activation mediated by toll-like receptor 4 attenuates angiotensin II-induced renal fibrosis and dysfunction.

Zheng XuChunpeng ZouWeihui YuSujing XuLan HuangZia KhanJingying WangGuang Liang Yi Wang

Published in: British journal of pharmacology (2019)

Our study reveals a novel mechanism of STAT3 activation, induced by angiotensin II, in kidney tissues and highlights a translational significance of a STAT3 inhibitor as potential therapeutic agent for hypertensive kidney disease.

Keyphrases

angiotensin ii
toll like receptor
angiotensin converting enzyme
vascular smooth muscle cells
cell proliferation
nuclear factor
inflammatory response
immune response
blood pressure
gene expression
high glucose
oxidative stress
drug induced