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Fibrosis and the bladder, implications for function ICI-RS 2017.

Christopher H Fry¹, Darry G Kitney¹, Jalesh Paniker²

¹School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, UK.

Neurourology and Urodynamics

|August 23, 2018

Summary

This summary is machine-generated.

Bladder fibrosis, an increase in extracellular matrix (ECM), impairs bladder function by replacing muscle tissue. Future research should focus on reducing ECM deposition to restore bladder contractility.

Keywords:

bladder contraction fibrosis

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Area of Science:

Urology
Pathology
Biomedical Engineering

Background:

Benign bladder pathologies often involve increased extracellular matrix (ECM) deposition, leading to fibrosis.
This fibrosis can alter matrix stiffness and impact bladder compliance and function.

Purpose of the Study:

To summarize current knowledge on the origins and consequences of bladder fibrosis.
To explore potential strategies for reducing fibrosis and restoring bladder function.

Main Methods:

Literature review and expert discussion at the International Consultation on Incontinence Research Society 2017 congress.
Analysis of PubMed literature to support arguments and derive proposals for future research.

Main Results:

Increased ECM deposition alters bladder tissue's elastic modulus, affecting urodynamic compliance.
Botulinum toxin injections showed no effect on compliance or fibrosis.
Transforming growth factor-beta (TGF-β) plays a key role in ECM deposition.
Reduced contractility is primarily due to detrusor muscle loss, not direct ECM interference.
Potential anti-fibrotic strategies include Vitamin-D, endostatin, relaxin, and epigenetic regulation of ECM.

Conclusions:

Reduced bladder contractility in fibrotic bladders is mainly caused by ECM replacing detrusor muscle.
Future research should target reducing ECM deposition to improve bladder function.