ArticleCell death & disease2018
M2 macrophage-mediated interleukin-4 signalling induces myofibroblast phenotype during the progression of benign prostatic hyperplasia.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
- Macrophage pyroptosis drives luminal senescence and club-cell reprogramming in 5α-reductase inhibitor-treated prostatic hyperplasia.Experimental & molecular medicine · 2026Article
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- Decoding benign prostatic hyperplasia at single-cell resolution: heterogeneity, inflammation, and beyond androgen-driven pathogenesis.Frontiers in immunology · 2026Review
- Article
- Nanomedicine for Benign Prostatic Hyperplasia: Pathological Axes and Translational Evidence.International journal of nanomedicine · 2026Review
- Fibroblasts promote the progression of benign prostatic hyperplasia through colony-stimulating factor 1 receptor-mediated RTK signaling in prostatic epithelial cells.Molecular biomedicine · 2025Article
- Salmonella enterica mediated epigenetic promotion of fibrosis is a novel factor in benign prostatic hyperplasia.Military Medical Research · 2025Article
- High dose methylprednisolone mediates YAP/TAZ-TEAD in vocal fold fibroblasts with macrophages.Scientific reports · 2025Article
- TRPML1 ion channel promotes HepaRG cell differentiation under simulated microgravity conditions.NPJ microgravity · 2025Article
- Comprehensive RNA-seq analysis of benign prostatic hyperplasia (BPH) in rats exposed to testosterone and estradiol.Scientific reports · 2025Article
- Prostatic Escherichia coli infection drives CCR2-dependent recruitment of fibrocytes and collagen production.Disease models & mechanisms · 2025Article
- Mechanisms of prostatic inflammation-mediated male lower urinary tract symptoms.American journal of clinical and experimental urology · 2025Review
- Defective autophagy of pericytes enhances radiation-induced senescence promoting radiation brain injury.Neuro-oncology · 2024Article
- IKKε-deficient macrophages impede cardiac repair after myocardial infarction by enhancing the macrophage-myofibroblast transition.Experimental & molecular medicine · 2024Article
- Androgen receptor deficiency-induced TUG1 in suppressing ferroptosis to promote benign prostatic hyperplasia through the miR-188-3p/GPX4 signal pathway.Redox biology · 2024Article
- Phosphodiesterase type 5 inhibitor tadalafil reduces prostatic fibrosis via MiR-3126-3p/FGF9 axis in benign prostatic hyperplasia.Biology direct · 2024Article
- Activation of the cGMP/PKG/ERK signaling pathway associated with PDE5Is inhibits fibroblast activation by downregulating autophagy in early progressive benign prostatic hyperplasia.World journal of urology · 2024Article
- Interleukin-4 from curcumin-activated OECs emerges as a central modulator for increasing M2 polarization of microglia/macrophage in OEC anti-inflammatory activity for functional repair of spinal cord injury.Cell communication and signaling : CCS · 2024Article
- Untargeted metabolomics reveals that declined PE and PC in obesity may be associated with prostate hyperplasia.PloS one · 2024Article
- Review
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Benign prostatic hyperplasia (BPH) is a progressive disease in elderly men, but potential factors accelerating its progression remain largely unknown. The aim of this study was to elucidate the factors affecting BPH progression by understanding the complex mechanisms causing early- progressed BPH, which progresses rapidly and requires surgical intervention before the age of 50. Three groups of human prostate tissue samples, from patients with early-progressed BPH, age-matched prostate and elderly BPH tissues, were collected (n = 25 each). We compared these tissues to determine the histologic features and molecular mechanisms underlying BPH progression. We found that early-progressed BPH samples were characterised by aberrant stromal hyper-proliferation, collagen deposition and increased M2 macrophage infiltration, compared to those from age-matched prostate and elderly BPH tissues. The M2 macrophage-fibroblast co-culture system demonstrated that the myofibroblast phenotypes were strongly induced only in fibroblasts from the early-progressed BPH samples, while the co-cultured M2 macrophages expressed high levels of pro-fibrotic cytokines, such as IL4 and TGFβ1. M2 macrophage-derived IL4, but not TGFβ1, selectively induced the myofibroblast phenotype through the JAK/STAT6, PI3K/AKT and MAPK/ERK signalling pathways in the early-progressed BPH prostate fibroblasts. Taken together, our results indicate that induction of the myofibroblast phenotype may lead to BPH progression through M2 macrophage-mediated IL4 signalling, and that IL4 may represent a potential therapeutic target, allowing the prevention of M2 macrophage activation and fibroblast-to-myofibroblast differentiation.
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