Dynamic Urothelial Remodeling in Diabetic Bladder Dysfunction: Disease-Course Changes, Molecular Mechanisms, and Clinical Implications
- 1School of Acupuncture-Moxibustion, Tuina and Rehabilitation, Hunan University of Chinese Medicine, Changsha 410208, China
Abstract
Diabetic bladder dysfunction (DBD) includes storage abnormalities and voiding dysfunction, but its clinical and experimental phenotypes do not follow a uniform chronological sequence. The urothelium is a urine barrier and a mechanosensory, paracrine, and inflammatory interface. Early diabetes may cause urothelial shedding, barrier permeability, abnormal ATP release, and altered sensory receptors. With longer disease duration, superficial architecture and some barrier properties may recover, while sensory and paracrine abnormalities persist. In parallel, impaired afferent conduction, reduced detrusor contractility, and extracellular matrix remodeling may become prominent, so local urothelial changes do not necessarily track whole-bladder function. Metabolic and oxidative stress, NLRP3-associated inflammation and pyroptosis, ferroptosis, and epigenetic and post-transcriptional regulation may contribute to urothelial injury, although evidence differs in cell specificity and disease-course localization. This review integrates clinical, animal, and cellular studies to examine urothelial barrier, sensory, paracrine, and cell-fate changes across DBD functional states, appraise the supporting molecular evidence and its limitations, and discuss the clinical relevance of urothelial biomarkers and therapeutic targets.
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BibTeX
@article{song2026dynamic,
title = {{Dynamic Urothelial Remodeling in Diabetic Bladder Dysfunction: Disease-Course Changes, Molecular Mechanisms, and Clinical Implications}},
author = {Quan Song and Wanjian Xie and Jing Wang and Yehuan Yuan and Zhi Li and Sisi Sun and Kun Ai},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27209033},
url = {https://www.mdpi.com/1422-0067/27/20/9033},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Dynamic Urothelial Remodeling in Diabetic Bladder Dysfunction: Disease-Course Changes, Molecular Mechanisms, and Clinical Implications
AU - Quan Song
AU - Wanjian Xie
AU - Jing Wang
AU - Yehuan Yuan
AU - Zhi Li
AU - Sisi Sun
AU - Kun Ai
PY - 2026
DA - 2026/10/12
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27209033
UR - https://www.mdpi.com/1422-0067/27/20/9033
AB - Diabetic bladder dysfunction (DBD) includes storage abnormalities and voiding dysfunction, but its clinical and experimental phenotypes do not follow a uniform chronological sequence. The urothelium is a urine barrier and a mechanosensory, paracrine, and inflammatory interface. Early diabetes may cause urothelial shedding, barrier permeability, abnormal ATP release, and altered sensory receptors. With longer disease duration, superficial architecture and some barrier properties may recover, while sensory and paracrine abnormalities persist. In parallel, impaired afferent conduction, reduced detrusor contractility, and extracellular matrix remodeling may become prominent, so local urothelial changes do not necessarily track whole-bladder function. Metabolic and oxidative stress, NLRP3-associated inflammation and pyroptosis, ferroptosis, and epigenetic and post-transcriptional regulation may contribute to urothelial injury, although evidence differs in cell specificity and disease-course localization. This review integrates clinical, animal, and cellular studies to examine urothelial barrier, sensory, paracrine, and cell-fate changes across DBD functional states, appraise the supporting molecular evidence and its limitations, and discuss the clinical relevance of urothelial biomarkers and therapeutic targets.
SN - 1422-0067
ER -