Bladder under stress : Pathological and adaptive shifts in channel expression
Swärd, Karl LU ; Andersson, Karl-Erik LU
and Uvelius, Bengt
LU
(2026)
In Channels
20(1).
- Abstract
Membrane channels are central to bladder function, yet current understanding is shaped disproportionately by a few well-studied families such as TRPA1 and TRPV1. To provide a more balanced view, this review analyzed emerging human transcriptomic datasets to identify the channels most highly expressed in the urinary bladder and examined how they remodel in bladder outlet obstruction and denervation. Sixty-seven channels were prominently expressed at the mRNA level in GTEx bladder tissue, with correlation analyses and protein expression data assigning many to smooth muscle, urothelial, endothelial, or neuronal compartments. Several abundant channels remain largely unstudied in urological contexts, including CLIC4, CLCN3, TPCN1 and ANO10.... (More)
Membrane channels are central to bladder function, yet current understanding is shaped disproportionately by a few well-studied families such as TRPA1 and TRPV1. To provide a more balanced view, this review analyzed emerging human transcriptomic datasets to identify the channels most highly expressed in the urinary bladder and examined how they remodel in bladder outlet obstruction and denervation. Sixty-seven channels were prominently expressed at the mRNA level in GTEx bladder tissue, with correlation analyses and protein expression data assigning many to smooth muscle, urothelial, endothelial, or neuronal compartments. Several abundant channels remain largely unstudied in urological contexts, including CLIC4, CLCN3, TPCN1 and ANO10. Disease-associated remodeling revealed shared and model-specific patterns. Outlet obstruction produced marked upregulation of L-type Ca2+ channel auxiliary subunits and robust changes in CLIC-family channels, whereas denervation induced broader channel downregulation not explained by nerve loss alone. Three channels, Gja1, Piezo1 and Ano1, were concordantly altered in both conditions, suggesting coordinated changes within interstitial cell networks and mechanotransductive pathways. These findings highlight a diverse and incompletely explored bladder "channel-ome." Expanding research beyond traditional targets may uncover new mechanisms underlying storage and voiding dysfunction and provide opportunities for therapeutic innovation in lower urinary tract disease.
(Less)
- author
- Swärd, Karl
LU
; Andersson, Karl-Erik
LU
and Uvelius, Bengt
LU
- organization
- publishing date
- 2026-12
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Humans, Urinary Bladder/metabolism, Ion Channels/metabolism, Animals
- in
- Channels
- volume
- 20
- issue
- 1
- article number
- 2652649
- publisher
- Taylor & Francis
- external identifiers
-
- pmid:41945411
- scopus:105035056767
- ISSN
- 1933-6950
- DOI
- 10.1080/19336950.2026.2652649
- language
- English
- LU publication?
- yes
- id
- fec3791a-d8d5-40c6-8008-3f94db2ee8da
- date added to LUP
- 2026-04-08 08:40:53
- date last changed
- 2026-06-01 04:00:33
@article{fec3791a-d8d5-40c6-8008-3f94db2ee8da,
abstract = {{<p>Membrane channels are central to bladder function, yet current understanding is shaped disproportionately by a few well-studied families such as TRPA1 and TRPV1. To provide a more balanced view, this review analyzed emerging human transcriptomic datasets to identify the channels most highly expressed in the urinary bladder and examined how they remodel in bladder outlet obstruction and denervation. Sixty-seven channels were prominently expressed at the mRNA level in GTEx bladder tissue, with correlation analyses and protein expression data assigning many to smooth muscle, urothelial, endothelial, or neuronal compartments. Several abundant channels remain largely unstudied in urological contexts, including CLIC4, CLCN3, TPCN1 and ANO10. Disease-associated remodeling revealed shared and model-specific patterns. Outlet obstruction produced marked upregulation of L-type Ca2+ channel auxiliary subunits and robust changes in CLIC-family channels, whereas denervation induced broader channel downregulation not explained by nerve loss alone. Three channels, Gja1, Piezo1 and Ano1, were concordantly altered in both conditions, suggesting coordinated changes within interstitial cell networks and mechanotransductive pathways. These findings highlight a diverse and incompletely explored bladder "channel-ome." Expanding research beyond traditional targets may uncover new mechanisms underlying storage and voiding dysfunction and provide opportunities for therapeutic innovation in lower urinary tract disease.</p>}},
author = {{Swärd, Karl and Andersson, Karl-Erik and Uvelius, Bengt}},
issn = {{1933-6950}},
keywords = {{Humans; Urinary Bladder/metabolism; Ion Channels/metabolism; Animals}},
language = {{eng}},
number = {{1}},
publisher = {{Taylor & Francis}},
series = {{Channels}},
title = {{Bladder under stress : Pathological and adaptive shifts in channel expression}},
url = {{http://dx.doi.org/10.1080/19336950.2026.2652649}},
doi = {{10.1080/19336950.2026.2652649}},
volume = {{20}},
year = {{2026}},
}