ArticleAmerican journal of clinical and experimental urology2020
Distinct cell-types in the prostate share an aging signature suggestive of metabolic reprogramming.
Article in American journal of clinical and experimental urology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Defining aging-associated factors that increase susceptibility to prostate cancer.Endocrine-related cancer · 2025Review
- Single-sEV profiling identifies the TACSTD2 + sEV subpopulation as a factor of tumor susceptibility in the elderly.Journal of nanobiotechnology · 2024Article
- Androgens, aging, and prostate health.Reviews in endocrine & metabolic disorders · 2022Review
- E-cadherin deficiency promotes prostate macrophage inflammation and bladder overactivity in aged male mice.Aging · 2022Article
- Aging of the progenitor cells that initiate prostate cancer.Cancer letters · 2021Review
- The Etiology and Pathophysiology Genesis of Benign Prostatic Hyperplasia and Prostate Cancer: A New Perspective.Medicines (Basel, Switzerland) · 2021Review
- The role of Trop2 in prostate cancer: an oncogene, biomarker, and therapeutic target.American journal of clinical and experimental urology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Age is a significant risk factor for disease of the prostate. However, the mechanisms by which age increases disease risk have not been well described. We previously reported age-related changes within the inflammatory and luminal compartments of the mouse prostate. Old mouse prostates exhibit an expansion of the population of Trop2+ luminal progenitor cells and a reduction in the frequency and functional capacity of Trop2- luminal cells, indicating that different cell-types have distinct responses to aging. Whether distinct cell-types in the prostate share a common signature of aging has not been established. We transcriptionally profiled four distinct cell-types in young adult and old mouse prostates: stromal, basal, Trop2+ luminal progenitor and Trop2- luminal cells. Motif analysis of genes upregulated in old prostate cell-types pointed to transcriptional regulators of inflammatory and hypoxia-related signaling. Glutathione metabolism and the antioxidant response emerged as a common signature of aging across prostatic lineages. Expression of genes implicated in mouse prostate aging, including the antioxidant response gene
Indexed as
Identifiers
32929410PMC7486537W3087744748What OpenQuestion 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 OpenQuestion graph.