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Updated: May 15, 2026
04:37
Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis
Published on: April 25, 2025
Renal nerves drive interstitial fibrogenesis in obstructive nephropathy
1Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska 68198-5850, USA.
Journal of the American Society of Nephrology : JASN
|December 25, 2012
Summary
Kidney nerve stimulation drives fibrosis after injury. Blocking nerve signals (norepinephrine and CGRP) prevents kidney fibrosis and inflammation, suggesting a new therapeutic target.
Area of Science:
- Nephrology
- Renal Pathophysiology
- Neuroscience
Background:
- Renal fibrogenesis mechanisms post-injury remain unclear.
- Understanding profibrotic signals is crucial for developing therapeutic strategies.
Purpose of the Study:
- To identify the primary signals driving kidney fibrosis after ureteral obstruction.
- To investigate the role of renal nerve stimulation in fibrogenesis.
Main Methods:
- Renal nerve stimulation and denervation models in kidneys.
- Local infusion of neural factors (norepinephrine, CGRP).
- Pharmacological blockade of α(2)-adrenergic and CGRP receptors.
Main Results:
- Renal nerve stimulation is identified as the primary profibrotic signal.
- Renal denervation effectively prevents kidney fibrosis and inflammation.
- Norepinephrine and CGRP mimic fibrotic responses via specific receptor pathways.
- Blocking these receptors inhibits fibrosis, inflammation, and tubular cell death.
Conclusions:
- Nerve-derived signaling molecules, specifically norepinephrine and CGRP, are key drivers of renal fibrosis.
- Targeting these nerve-derived signals offers a potential therapeutic strategy for preventing kidney fibrosis.
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