ArticleFrontiers in immunology2025
Immune cell single-cell RNA sequencing analyses link an age-associated T cell subset to symptomatic benign prostatic hyperplasia.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Immune dysregulation in the prostates of C57BL/6The Journal of pathology · 2026Article
- T cell-derived CCL5 drives macrophage immunometabolic remodeling in chronic prostatitis via the CCR5-ERK-PKM2/HIF-1α axis.Redox biology · 2026Article
- Global stagnation and misaligned priorities in BPH drug development: a 25-year landscape analysis of clinical trial registries.npj aging · 2026Article
- Decoding benign prostatic hyperplasia at single-cell resolution: heterogeneity, inflammation, and beyond androgen-driven pathogenesis.Frontiers in immunology · 2026Review
- Investigation of the association of tRNA-derived fragments (tRF-17-79MP9PP and tRF-18-79MP9P04) with prostate cancer.Molecular biology reports · 2025Article
- Integrated management strategies for benign prostatic hyperplasia.Frontiers in urology · 2025Review
- Involvement of SIRT1-mediated aging in liver diseases.Frontiers in cell and developmental biology · 2025Review
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Abstract
Introduction: Benign prostatic hyperplasia (BPH) is among the most common age-associated diseases in men. Prostatic immune cell infiltration is frequently observed with aging coincident with BPH; however, the contribution of age-related changes in immune cells to BPH is not clear. As T cells are the predominate immune cell in aged prostates, it is hypothesized that age-associated alterations in T cell subsets contribute to BPH symptoms. Methods: scRNA-seq data from immune cells isolated from small (≤40g) and large (≥90g) prostates from aged men (>50 years) were combined with previously published scRNA-seq data from three young organ donor prostates to compare young to aged prostate T cells and small to large aged prostate T cells. Cycling and senescent BPH patient-derived fibroblasts were treated with granzyme K and senescence-associated secretory phenotype (SASP)-associated cytokines were measured by ELISA. Results: An age-associated CD8 Discussion: These data suggest that granzyme K-mediated stimulation of prostate stromal fibroblast SASP cytokine and chemokine production promotes prostate immune cell recruitment and activation. Overall, these results connect symptomatic BPH with immune aging.
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