Factors contributing to bladder fibrosis
Swärd, Karl LU ; Andersson, Karl Erik LU
and Uvelius, Bengt
LU
(2025)
In Continence
14.
- 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... (More)
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.
(Less)
- author
- Swärd, Karl
LU
; Andersson, Karl Erik
LU
and Uvelius, Bengt
LU
- organization
- publishing date
- 2025-06
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Collagen, Fibrosis, Hypoxia, Obstruction, Urinary bladder
- in
- Continence
- volume
- 14
- article number
- 101763
- publisher
- Elsevier
- external identifiers
-
- scopus:105004050549
- ISSN
- 2772-9737
- DOI
- 10.1016/j.cont.2025.101763
- language
- English
- LU publication?
- yes
- id
- c4f1c57f-9b74-442d-bb7c-38ee9863c5fa
- date added to LUP
- 2025-07-30 11:43:40
- date last changed
- 2025-07-30 11:44:21
@article{c4f1c57f-9b74-442d-bb7c-38ee9863c5fa,
abstract = {{<p>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.</p>}},
author = {{Swärd, Karl and Andersson, Karl Erik and Uvelius, Bengt}},
issn = {{2772-9737}},
keywords = {{Collagen; Fibrosis; Hypoxia; Obstruction; Urinary bladder}},
language = {{eng}},
publisher = {{Elsevier}},
series = {{Continence}},
title = {{Factors contributing to bladder fibrosis}},
url = {{http://dx.doi.org/10.1016/j.cont.2025.101763}},
doi = {{10.1016/j.cont.2025.101763}},
volume = {{14}},
year = {{2025}},
}