ArticleInternational urogynecology journal2025
Regulation of Autophagy by the Cdk1/p53/p21 Feedback Loop in an Interstitial Cystitis/Bladder Pain Syndrome Cell Model: Implications for Inflammatory Response.
Article in International urogynecology journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Cellular Senescence and SASP in Bladder Ageing: Mechanisms and Emerging Interventions.International journal of general medicine · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
introduction and hypothesisThe Cdk1/p53/p21 feedback loop could play an important role in maintaining a consistently high urinary tract epithelial permeability. This study is aimed at elucidating whether this feedback loop is associated with the inadequate autophagic response and the heightened inflammatory response in interstitial cystitis/bladder pain syndrome (IC/BPS).
methodsTo construct the IC/BPS cell model, HTB4 cells were first treated with 1% H
resultsCompared with normal urothelial HTB4 cells, the number of autophagosomes and the levels of LC3-I/II and Beclin 1 are significantly increased in IC/BPS cells. These cells also exhibit markedly higher levels of inflammatory markers (TNFα, IL-6, IL-8) and MDA, alongside notably reduced levels of the antioxidants GSH and SOD2. Compared with IC/BPS cells or IC/BPS cells co-transfected with p21 siRNA and Cdk1 control, the IC/BPS cells co-transfected with p21 siRNA and Cdk1 inhibitor exhibit a significant increase in terms of autophagosome numbers and the LC3-I/II level. Additionally, the levels of inflammatory factors are significantly decreased in the IC/BPS cells co-transfected with p21 siRNA and Cdk1 inhibitor.
conclusionIn IC/BPS, the Cdk1/p53/p21 feedback loop could regulate the level of autophagy and inflammatory response. This discovery identifies promising new therapeutic targets for IC/BPS, which may pave the way for innovative clinical approaches to this complex disorder.
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Registered trials
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