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Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
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Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

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

Zheng Xu1, Chunpeng Zou2, Weihui Yu3

  • 1Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.

British Journal of Pharmacology
|April 9, 2019
PubMed
Abstract

Insights

Angiotensin II activates STAT3 in kidney cells via toll-like receptor 4, driving kidney disease progression. Inhibiting STAT3 offers a potential therapy for hypertension-related kidney damage.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Hypertension is a leading cause of kidney failure.
  • Angiotensin II contributes to hypertensive kidney disease progression.
  • STAT3 activation by Angiotensin II in kidneys is not well understood.

Purpose of the Study:

  • Investigate the mechanism of STAT3 activation by Angiotensin II in kidney cells.
  • Determine the functional consequences of STAT3 activation in hypertensive kidney disease.
  • Evaluate STAT3 inhibition as a therapeutic strategy.

Main Methods:

  • Angiotensin II infusion in mice to induce nephropathy.
  • STAT3 inhibition using shRNA or S3I-201.
  • In vitro studies with renal proximal tubular cells.
  • Analysis of human kidney samples.

Main Results:

  • Angiotensin II activated STAT3 in kidney cells via TLR4 and JAK2, independent of IL-6/gp130 and AT1 receptors.
  • STAT3 activation led to increased fibrotic proteins and renal dysfunction.
  • STAT3 inhibition and TLR4 deficiency normalized kidney fibrosis and dysfunction without affecting blood pressure.

Conclusions:

  • A novel mechanism of Angiotensin II-induced STAT3 activation in kidneys was identified.
  • STAT3 inhibition shows potential as a therapeutic approach for hypertensive kidney disease.

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