ArticleAmerican journal of clinical and experimental urology2020
Transforming growth factor beta 1 impairs benign prostatic luminal epithelial cell monolayer barrier function.
Article in American journal of clinical and experimental urology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Lipid and Foam Cell Accumulation as Novel Pathological Features of Benign Prostatic Hyperplasia.The Prostate · 2026Article
- Article
- The Effects of 1,8-Cineole Treatment on Benign Prostatic Hyperplasia in Rats.Current pharmaceutical biotechnology · 2026Article
- Ripasudil, a Rho kinase inhibitor, attenuates testosterone-induced benign prostatic hyperplasia in rats: targeting inflammation, oxidative stress, and Rho kinase pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Paeonol Ameliorates Benign Prostatic Hyperplasia via Suppressing Proliferation and NF-κB-In Silico and Experimental Studies.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Exploring TGF-β signaling in benign prostatic hyperplasia: from cellular senescence to fibrosis and therapeutic implications.Biogerontology · 2025Review
- The Blood-prostate Barrier: An Obstacle to Drug Delivery into the Prostate.Current drug delivery · 2025Review
- Characterization of prostate macrophage heterogeneity, foam cell markers, and CXCL17 upregulation in a mouse model of steroid hormone imbalance.Scientific reports · 2024Article
- Chronic inflammation in benign prostatic hyperplasia: Pathophysiology and treatment options.International journal of urology : official journal of the Japanese Urological Association · 2024Review
- PROSTATE CELL HETEROGENEITY AND CXCL17 UPREGULATION IN MOUSE STEROID HORMONE IMBALANCE.bioRxiv : the preprint server for biology · 2024Article
- Bioassay-guided isolation of two antiproliferative metabolites fromFrontiers in pharmacology · 2024Article
- Article
- Effects of red ginseng oil(KGC11Journal of ginseng research · 2022Article
- E-cadherin expression is inversely correlated with aging and inflammation in the prostate.American journal of clinical and experimental urology · 2021Article
- Claudin-1 down-regulation in the prostate is associated with aging and increased infiltration of inflammatory cells in BPH.American journal of clinical and experimental urology · 2021Article
- HMGB1 enhances epithelial permeability via p63/TGF-β signaling in lung and terminal bronchial epithelial cells.Tissue barriers · 2020Article
- Tight junction protein claudin-1 is downregulated by TGF-β1 via MEK signaling in benign prostatic epithelial cells.The Prostate · 2020Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Our recent studies identifying the presence of luminal secretory protein PSA in the stroma, decreased E-cadherin expression, and reduced number of tight junction kiss points in benign prostatic hyperplasia (BPH) tissues suggest that epithelial barrier permeability is increased in BPH. However, the cause of increased epithelial permeability in BPH is unclear. Transforming growth factor beta 1 (TGF-β1) has been reported to be up-regulated in clinical BPH specimens and TGF-β1 overexpression induced fibrosis and inflammation in a murine model. TGF-β1 was reported to repress the expression of E-cadherin in benign prostatic cells. However, whether and how TGF-β1 up-regulation affects epithelial barrier permeability is unknown. Here,
Indexed as
Identifiers
32211449PMC7076294W3015969726What 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.