Factors contributing to bladder fibrosis

Abstract

Background:

Bladder outlet obstruction, commonly resulting from benign prostatic hyperplasia or congenital urethral valves, is a prevalent cause of voiding dysfunction. This condition induces significant bladder hypertrophy, alters excitability, and increases residual urine. Obstruction has been extensively studied in experimental animal models using surgical obstruction. A frequent pathological endpoint is bladder fibrosis, characterized by structural and functional deterioration of the bladder wall

Objective:

This article examines the pathophysiological mechanisms linking bladder outlet obstruction to fibrosis, with particular attention to bladder wall overstretch, compromised perfusion, and neural impairment

Methods:

We conducted a targeted literature review, employing search terms including urinary bladder, obstruction, hypoxia, and fibrosis. In addition, we analysed a bank of electron micrographs and publicly available microarray datasets derived from obstructed rat bladders to support our synthesis of experimental findings

Key Findings:

Our analysis underscores the intricate interplay among mechanical forces, neural input, and molecular signalling in the pathogenesis of bladder fibrosis secondary to outlet obstruction. We present a flow chart that models fibrosis progression in obstructed rat bladders. This algorithm synthesizes experimental data and incorporates key parameters such as bladder wall tension, hemodynamics, inflammatory cytokine levels, leading to expression of fibrosis-driving proteins.

Conclusions:

The proposed model offers a conceptual and analytical framework for studying fibrosis in the context of bladder outlet obstruction. It holds promise for guiding future research and informing the development of targeted therapeutic strategies aimed at interrupting the progression of bladder dysfunction driven by ischemia, oxidative stress, and chronic inflammation.