ArticleIn vitro cellular & developmental biology. Animal2024
TGFβ2 mediates oxidative stress-induced epithelial-to-mesenchymal transition of bladder smooth muscle.
Article in In vitro cellular & developmental biology. Animal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 1 citations in OpenAlex.
- Oxidative stress in bladder outlet obstruction: a narrative review.Translational andrology and urology · 2026Review
- Corydaline overcomes doxorubicin resistance in oral cancer by activating the p53-Bax-caspase axis and inhibiting MMP-driven invasion: an in vitro, in vivo, and in silico study.In vitro cellular & developmental biology. Animal · 2026Article
- Prospective observational study of oxidative stress in the pathology of benign prostatic hyperplasia with bladder diverticulum.PloS one · 2025Observational
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Bladder outlet obstruction (BOO) is the primary clinical manifestation of benign prostatic hyperplasia, the most common urinary system disease in elderly men, and leads to associated lower urinary tract symptoms. Although BOO is reportedly associated with increased systemic oxidative stress (OS), the underlying mechanism remains unclear. The elucidation of this mechanism is the primary aim of this study. A Sprague-Dawley rat model of BOO was constructed and used for urodynamic monitoring. The bladder tissue of rats was collected and subjected to real-time reverse transcription-quantitative polymerase chain reaction (RT-qPCR), histological examination, and immunohistochemical staining. Through bioinformatics prediction, we found that transforming growth factor β2 (TGFβ2) expression was upregulated in rats with BOO compared with normal bladder tissue. In vitro analyses using primary bladder smooth muscle cells (BSMCs) revealed that hydrogen peroxide (H
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