ReviewBiogerontology2025
Exploring TGF-β signaling in benign prostatic hyperplasia: from cellular senescence to fibrosis and therapeutic implications.
Review in Biogerontology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed.
- Article
- Global stagnation and misaligned priorities in BPH drug development: a 25-year landscape analysis of clinical trial registries.npj aging · 2026Article
- Mechanistic insights into the anti-benign prostatic hyperplasia effect of dihydromyricetin via suppression of the 5-AR/TGF-β1/Smad2 axis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Review
- Prostatitis-Related Male Infertility: From Inflammation and Dysbiosis to Sperm DNA Damage.Diagnostics (Basel, Switzerland) · 2026Review
- Decoding benign prostatic hyperplasia at single-cell resolution: heterogeneity, inflammation, and beyond androgen-driven pathogenesis.Frontiers in immunology · 2026Review
- The impact of dietary inflammation index on benign prostatic hyperplasia: insights from patient data and animal models.Frontiers in nutrition · 2026Article
- Pathophysiological mechanisms of benign prostatic obstruction in men with small prostate volume and the emerging role of ultra-minimally invasive prostatic urethral dilation: a narrative review.Frontiers in molecular biosciences · 2026Review
- Resveratrol in benign prostatic hyperplasia: mechanistic insights and therapeutic perspectives.Frontiers in immunology · 2026Review
- Liver fibrosis is associated with men's health care symptoms, especially erectile dysfunction and lower urinary tract symptoms.Investigative and clinical urology · 2025Article
- TNF-α modulates cell proliferation via SOX4/TGF-β/Smad signaling in benign prostatic hyperplasia.Cell death & disease · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As men get older, they often develop benign prostatic hyperplasia (BPH), an enlarged prostate that is not cancerous or dangerous. Although the etiology of BPH is unknown, increasing evidence indicates that the TGF-β signaling pathway might be a key player in its pathogenesis. TGF-β is a pleiotropic cytokine involved in proliferation, differentiation, and extracellular matrix re-modeling, which are all dysregulated in BPH. Cellular senescence is primarily initiated by TGF-β--induced, irreversible growth arrest and usually limits the prostate gland's hyperplastic growth. Moreover, senescent cells generate a Senescence-Associated Secretory Phenotype (SASP), which consists of numerous proinflammatory and profibrotic factors that can worsen disease ontogeny. In addition, TGF-β is among the most fibrogenic factors. At the same time, fibrosis involves a massive accumulation of extracellular matrix proteins, which can increase tissue stiffness and a loss of normal organ functions. TGF-β-mediated fibrosis in BPH changes the mechanical properties of the prostate and surrounding tissues to contribute to lower urinary tract symptoms. This review discusses the complicated molecular signaling of TGF-β underlying changes in cellular senescence and fibrosis during BPH concerning its therapeutic potential.
Indexed as
Identifiers
40159577What Socratic 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 Socratic graph.