ArticleCommunications biology2026
Wnt11 mediates fibroblast-smooth muscle cell interaction to promote neurogenic bladder fibrosis in rats.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed.
- Biomechanical regulation of bladder injury and repair.Nature reviews. Urology · 2026Review
- Piezo1 promote macrophage-to-myofibroblast transition and bladder fibrosis in neurogenic bladder.World journal of urology · 2026Article
- Genetic Modulation of Wound Healing Pathways and Postoperative Risk in Plastic and Reconstructive Surgery: A Cohort Study.Journal of clinical medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Neurogenic bladder (NB) is a lower urinary tract dysfunction caused by lesions in the nervous system that regulate urine storage and micturition. Fibrosis is considered the basic pathological alteration of NB, whereas the underlying mechanism remains unclear. Here, we find that Wnt11 is significantly up-regulated in the rat fibrotic bladders induced by bilateral pelvic nerve injury (BPNI) and spinal cord injury (SCI) and promotes bladder fibroblasts (BFs)-to-myofibroblasts transition and smooth muscle cells (SMCs) phenotypic transformation. Selective inhibition or gene silencing of Wnt11 in vivo and in vitro attenuates BFs and SMCs activation, and mitigates the development of NB fibrosis. Mechanistically, Wnt11 specifically binds to Vangl2 receptor to activate downstream JNK/c-JUN signaling via the membrane recruitment of DVL2. Further research shows that Wnt11 signaling interacts with transforming growth factor beta 1 (TGF-β1)/Smad-dependent pathway through the binding of membrane receptors (Vangl2 and TβR1) and the crosstalk of nuclear transcription factors. These findings uncover the regulatory mechanism and may provide a new therapeutic strategy for NB fibrosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.