ArticlePloS one2012
CXC-type chemokines promote myofibroblast phenoconversion and prostatic fibrosis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Metabolic syndrome, inflammation and lower urinary tract symptoms: possible translational links.Prostate cancer and prostatic diseases · 2016Pooled it
- Prostate Transition Zone Fibrosis is Associated with Clinical Progression in the MTOPS Study.The Journal of urology · 2019Trial
- Lipid and Foam Cell Accumulation as Novel Pathological Features of Benign Prostatic Hyperplasia.The Prostate · 2026Article
- Antifibrotic therapy for Lower Urinary Tract Symptoms secondary to Benign Prostatic Hyperplasia.Prostate cancer and prostatic diseases · 2026Review
- Dysregulated Cell Signaling Pathways in Prostate Tumoral Plasticity-Checkpoints.Oncology research · 2026Article
- Nanomedicine for Benign Prostatic Hyperplasia: Pathological Axes and Translational Evidence.International journal of nanomedicine · 2026Review
- Bidirectional Interaction Between PGEProteomes · 2025Article
- Sestrin2 ameliorates age-related spontaneous benign prostatic hyperplasia via activation of AMPK/mTOR dependent autophagy.Biogerontology · 2025Article
- Mechanisms of prostatic inflammation-mediated male lower urinary tract symptoms.American journal of clinical and experimental urology · 2025Review
- Prostatic Escherichia coli infection drives CCR2-dependent recruitment of fibrocytes and collagen production.Disease models & mechanisms · 2025Article
- CXCR4 regulates macrophage M1 polarization by altering glycolysis to promote prostate fibrosis.Cell communication and signaling : CCS · 2024Article
- Characterization of prostate macrophage heterogeneity, foam cell markers, and CXCL17 upregulation in a mouse model of steroid hormone imbalance.Scientific reports · 2024Article
- The multifaceted role of the stroma in the healthy prostate and prostate cancer.Journal of translational medicine · 2024Review
- Radiology of fibrosis part III: genitourinary system.Journal of translational medicine · 2024Review
- PROSTATE CELL HETEROGENEITY AND CXCL17 UPREGULATION IN MOUSE STEROID HORMONE IMBALANCE.bioRxiv : the preprint server for biology · 2024Article
- Inhibition of bromodomain regulates cellular senescence in pancreatic adenocarcinoma.International journal of clinical and experimental pathology · 2024Article
- A Bayesian noisy logic model for inference of transcription factor activity from single cell and bulk transcriptomic data.NAR genomics and bioinformatics · 2023Article
- The Emerging Role of Cell Adhesion Molecules on Benign Prostatic Hyperplasia.International journal of molecular sciences · 2023Review
- The Symptoms of Benign Prostatic Hyperplasia Patients with Stromal-Dominated Hyperplasia Nodules May Be Associated with Prostate Fibrosis.International journal of general medicine · 2023Article
- The impact of short term, long term and intermittentAmerican journal of clinical and experimental urology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Recent studies from our group suggest that extracellular matrix (ECM) deposition and fibrosis characterize the peri-urethral prostate tissues of some men suffering from Lower Urinary Tract Symptoms (LUTS) and that fibrosis may be a contributing factor to the etiology of LUTS. Fibrosis can generally be regarded as an errant wound-healing process in response to chronic inflammation, and several studies have shown that the aging prostate tissue microenvironment is rich with inflammatory cells and proteins. However, it is unclear whether these same inflammatory proteins, particularly CXC-type chemokines, can mediate myofibroblast phenoconversion and the ECM deposition necessary for the development of prostatic tissue fibrosis. To examine this, immortalized and primary prostate stromal fibroblasts treated with TGF-β1, CXCL5, CXCL8, or CXCL12 were evaluated morphologically by microscopy, by immunofluorescence and qRT-PCR for αSMA, collagen 1, vimentin, calponin, and tenascin protein and transcript expression, and by gel contraction assays for functional myofibroblast phenoconversion. The results of these studies showed that that immortalized and primary prostate stromal fibroblasts are induced to express collagen 1 and 3 and αSMA gene transcripts and proteins and to undergo complete and functional myofibroblast phenoconversion in response to CXC-type chemokines, even in the absence of exogenous TGF-β1. Moreover, CXCL12-mediated myofibroblast phenoconversion can be completely abrogated by inhibition of the CXCL12 receptor, CXCR4. These findings suggest that CXC-type chemokines, which comprise inflammatory proteins known to be highly expressed in the aging prostate, can efficiently and completely mediate myofibroblast phenoconversion and may thereby promote fibrotic changes in prostate tissue architecture associated with the development and progression of male lower urinary tract dysfunction.
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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.