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Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis
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Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis

Published on: April 25, 2025

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AXL targeting reduces fibrosis development in experimental unilateral ureteral obstruction

Lea Landolt1, Jessica Furriol2, Janka Babickova1

  • 1Department of Clinical Medicine, University of Bergen, Bergen, Norway.

Physiological Reports
|May 29, 2019
PubMed

Insights

AXL receptor inhibition with bemcentinib reduced kidney fibrosis and inflammation in mice with unilateral ureteral obstruction. This suggests AXL receptor tyrosine kinase (RTK) is a promising therapeutic target for treating kidney fibrosis.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pharmacology

Background:

  • Renal fibrosis is a major cause of kidney disease progression.
  • Epithelial-to-mesenchymal transition (EMT) and inflammation are key drivers of renal fibrosis.
  • AXL receptor tyrosine kinase (RTK) signaling is implicated in EMT and inflammation.

Purpose of the Study:

  • To investigate the therapeutic potential of AXL inhibition in a mouse model of kidney fibrosis.
  • To evaluate the effects of bemcentinib, an AXL inhibitor, on fibrosis and inflammation markers following unilateral ureteral obstruction (UUO).

Main Methods:

  • Unilateral ureteral obstruction (UUO) model in C57BL/6 mice.
  • Treatment groups included bemcentinib, ACE inhibitor (ACEI), combined ACEI and bemcentinib, and vehicle control.
  • Kidney tissues analyzed via immunohistochemistry (IHC), western blot, ELISA, Sirius Red staining, hydroxyproline quantification, and RNA sequencing.

Main Results:

  • Bemcentinib treatment significantly reduced kidney fibrosis, as evidenced by Sirius Red staining and hydroxyproline levels.
  • AXL inhibition decreased markers of (partial) epithelial-to-mesenchymal transition (EMT), including Vimentin (VIM), alpha smooth muscle actin (αSMA), and key EMT regulators.
  • Bemcentinib treatment also reduced inflammatory infiltrates, indicated by lower F4/80 positive cells and inflammatory chemokines (MCP1, MCP3, MCP5, TARC).

Conclusions:

  • AXL receptor tyrosine kinase (RTK) signaling blockade with bemcentinib effectively ameliorates kidney fibrosis and associated inflammation.
  • AXL RTK inhibition demonstrates significant therapeutic potential for managing kidney fibrosis.
  • Targeting the AXL RTK pathway offers a promising strategy for pharmacologic intervention in kidney fibrosis.
Keywords:
UUOAXL targetingBemcentinib (BGB324)renal fibrosis

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