Evidence map›Paper›PMID 40949435›Full record

ReviewTranslational andrology and urology2025

A scoping review of the role of heritability and environmental exposures in the development and severity of benign prostatic hyperplasia.

Seyedeh Sima Daryabari, Kiarad Fendereski, Matthew D Grimes, Kelli X Gross, Stephen Summers, Joemy M Ramsay, Jeremy B Myers

Abstract readReview
In one paragraph

Review in Translational andrology and urology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Seyedeh Sima DaryabariDivision of Urology, Department of Surgery, University of Utah, Salt Lake City, UT, USA.
Kiarad FendereskiDivision of Urology, Department of Surgery, University of Utah, Salt Lake City, UT, USA.
Matthew D GrimesDepartment of Urology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Kelli X GrossDivision of Urology, Department of Surgery, University of Utah, Salt Lake City, UT, USA.
Stephen SummersDivision of Urology, Department of Surgery, University of Utah, Salt Lake City, UT, USA.
Joemy M RamsayDivision of Urology, Department of Surgery, University of Utah, Salt Lake City, UT, USA.
Jeremy B MyersDivision of Urology, Department of Surgery, University of Utah, Salt Lake City, UT, USA.

Funding

Wisconsin Multidisciplinary K12 Urologic Research Career Development ProgramK12DK100022 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI CHAD M. VEZINA · 2013 to 2026
$8.6M
NIDDK NIH HHS K12 DK100022
6 · The paper itself

Abstract

Background: Benign prostatic hyperplasia (BPH) is a common condition among aging men, significantly affecting quality of life and contributing to a substantial healthcare burden. The pathogenesis of BPH is strongly influenced by genetic factors, with heritability estimates showing a wide range from 20% to 83%. Emerging evidence also highlights the critical role of environmental exposures, including endocrine-disrupting chemicals (EDCs), in BPH risk, progression, and therapeutic response. This review synthesizes current knowledge on genetic and environmental determinants of BPH pathogenesis, severity, and management. Methods: A scoping review of the literature was conducted using the databases PubMed, Scopus, and Web of Science. Relevant studies on genetic predisposition, environmental exposures, and their contributions to BPH were analyzed. Data from epidemiological studies, genome-wide association studies (GWAS), familial aggregation analyses, and research on environmental exposures were integrated to provide an understanding of these factors and BPH pathogenesis. Results: Familial clustering indicates a significantly elevated risk, particularly among first-degree male relatives. Key genetic determinants include androgen receptor ( Conclusions: The development and progression of BPH are shaped by a complex interplay of genetic and environmental factors. EDCs contribute significantly to prostatic hyperplasia, while heritable factors influence disease onset, severity, and response to treatment. Integrating genetic risk profiling and environmental exposure assessments into clinical practice holds the potential to enhance BPH management and personalized therapeutic strategies.

Indexed as

Benign prostatic hyperplasia (BPH)endocrine-disrupting chemicals (EDCs)geneticgenetic predispositionpolymorphism

Identifiers

PMID40949435
PMCPMC12433160

What OpenQuestion holds

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Registered trials

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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.