ArticleCell death & disease2022
Estrogen and G protein-coupled estrogen receptor accelerate the progression of benign prostatic hyperplasia by inducing prostatic fibrosis.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 64 citations in OpenAlex.
- KDM4A drives TGCT metastasis by inducing focal adhesion disassembly via STAT1-mediated CCL3 transcriptional activation.Oncogene · 2026Article
- Article
- Elevated Estradiol and DHT Levels in the Prostatic Stroma as Key Drivers of Benign Prostatic Hyperplasia Pathogenesis.International journal of molecular sciences · 2026Article
- Association between dynamic abdominal obesity (DAO) and benign prostatic hyperplasia (lower urinary tract symptoms): evidence from the China Health and Retirement Longitudinal Study (CHARLS).World journal of urology · 2026Article
- Association between the G-protein-coupled estrogen receptor 1 and prostate cancer in the Slovak population.Molecular biology reports · 2026Article
- JMJD3 modulates benign prostatic hyperplasia through epigenetic regulation of TGF-β1.Cell death & disease · 2026Article
- Green chemistry for prostate health: exploring nature's toolbox against cancer, inflammation, and hyperplasia.Molecular diversity · 2026Review
- miR-16-5p mediates E2-induced cell proliferation and EMT in benign prostate hyperplasia.Scientific reports · 2026Article
- Anti-hyperplastic effects of Acmella oleracea flower and leaf extracts in prostate cell lines and in spontaneously hypertensive rats.Journal of molecular histology · 2026Article
- Estrogen regulation in the prostate underlies racial disparity in men with benign prostatic hyperplasia.The Journal of pathology · 2026Article
- Overexpression of GPER1 suppressed esophageal carcinoma growthEuropean journal of histochemistry : EJH · 2026Article
- Liver fibrosis is associated with men's health care symptoms, especially erectile dysfunction and lower urinary tract symptoms.Investigative and clinical urology · 2025Article
- Pleiotrophin modulates cell proliferation, prostate smooth muscle contraction and fibrosis in hyperplastic prostate.Journal of translational medicine · 2025Article
- Phytochemical characterization and therapeutic mechanism of Xialiqi capsule on benign prostatic hyperplasia.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- A scoping review of the role of heritability and environmental exposures in the development and severity of benign prostatic hyperplasia.Translational andrology and urology · 2025Review
- Sex-Dependent Regulation of Liver Fibrosis in Primary Sclerosing Cholangitis: The Role of miR-125b, Androgen Receptors, TGF-β, and Apelin Signalling.International journal of molecular sciences · 2025Article
- Salmonella enterica mediated epigenetic promotion of fibrosis is a novel factor in benign prostatic hyperplasia.Military Medical Research · 2025Article
- SIGMAR1 screened by a GPCR-related classifier regulates endoplasmic reticulum stress in bladder cancer.Journal of translational medicine · 2025Article
- Exploring TGF-β signaling in benign prostatic hyperplasia: from cellular senescence to fibrosis and therapeutic implications.Biogerontology · 2025Review
- Smooth muscle contractility of laser-enucleated prostate tissues and impacts of preoperative αScientific reports · 2025Article
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Benign prostatic hyperplasia (BPH) is the most common and progressive urological disease in elderly men worldwide. Epidemiological studies have suggested that the speed of disease progression varies among individuals, while the pathophysiological mechanisms of accelerated clinical progression in some BPH patients remain to be elucidated. In this study, we defined patients with BPH as belonging to the accelerated progressive group (transurethral resection of the prostate [TURP] surgery at ≤50 years old), normal-speed progressive group (TURP surgery at ≥70 years old), or non-progressive group (age ≤50 years old without BPH-related surgery). We enrolled prostate specimens from the three groups of patients and compared these tissues to determine the histopathological characteristics and molecular mechanisms underlying BPH patients with accelerated progression. We found that the main histopathological characteristics of accelerated progressive BPH tissues were increased stromal components and prostatic fibrosis, which were accompanied by higher myofibroblast accumulation and collagen deposition. Mechanism dissection demonstrated that these accelerated progressive BPH tissues have higher expression of the CYP19 and G protein-coupled estrogen receptor (GPER) with higher estrogen biosynthesis. Estrogen functions via GPER/Gαi signaling to modulate the EGFR/ERK and HIF-1α/TGF-β1 signaling to increase prostatic stromal cell proliferation and prostatic stromal fibrosis. The increased stromal components and prostatic fibrosis may accelerate the clinical progression of BPH. Targeting this newly identified CYP19/estrogen/GPER/Gαi signaling axis may facilitate the development of novel personalized therapeutics to better suppress the progression of BPH.
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