ReviewJournal of endocrinological investigation2014
Benign prostatic hyperplasia: a new metabolic disease?
Review in Journal of endocrinological investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 4 of them syntheses that pooled 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.
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
79 citing papers in PubMed, 4 syntheses or guidelines pooled it, 170 citations in OpenAlex.
- Immune Cell Proinflammatory Microenvironment and Androgen-Related Metabolic Regulation During Benign Prostatic Hyperplasia in Aging.Frontiers in immunology · 2022Pooled it
- Role of CYP17 rs743572 Polymorphism in Benign Prostatic Hyperplasia: A Multivariate Integrated Analysis.Frontiers in physiology · 2019Pooled it
- Molecular correlates in urine for the obesity and prostatic inflammation of BPH/LUTS patients.The Prostate · 2018Pooled it
- Meta-analysis of metabolic syndrome and prostate cancer.Prostate cancer and prostatic diseases · 2017Pooled it
- Testosterone does not affect lower urinary tract symptoms while improving markers of prostatitis in men with benign prostatic hyperplasia: a randomized clinical trial.Journal of endocrinological investigation · 2022Trial
- Preclinical animal models of lower urinary tract dysfunction associated with metabolic syndrome.Nature reviews. Urology · 2026Review
- The role of phosphatidylinositol (18:1_18:1) in benign prostatic hyperplasia: an integrated study of Mendelian randomization and network pharmacology.World journal of urology · 2025Article
- TNF-α modulates cell proliferation via SOX4/TGF-β/Smad signaling in benign prostatic hyperplasia.Cell death & disease · 2025Article
- Association between the Chinese Visceral Adiposity Index and the risk of Benign Prostatic Hyperplasia: a national prospective cohort study.Scientific reports · 2025Article
- Immune cell single-cell RNA sequencing analyses link an age-associated T cell subset to symptomatic benign prostatic hyperplasia.Frontiers in immunology · 2025Article
- Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia.Biology · 2024Article
- A genetic study to identify pathogenic mechanisms and drug targets for benign prostatic hyperplasia: a multi-omics Mendelian randomization study.Scientific reports · 2024Article
- Hypoxia activates the hypoxia-inducible factor-1α/vascular endothelial growth factor pathway in a prostatic stromal cell line: A mechanism for the pathogenesis of benign prostatic hyperplasia.Current urology · 2024Article
- Is There an Association between 5a Reductase Inhibitors and Metabolic Syndrome? A Narrative Review of the Literature.Reviews on recent clinical trials · 2024Review
- Exploring the potential mechanism of Xiaojin Pill therapy for benign prostatic hyperplasia through metabolomics and gut microbiota analysis.Frontiers in microbiology · 2024Article
- Gestational exposure to the great Chinese famine: early life undernutrition impact on prostatic hyperplasia in adulthood.Frontiers in nutrition · 2024Article
- Long-Term Exposure to Supraphysiological Levels of Testosterone Impacts Rat Submandibular Gland Proteome.International journal of molecular sciences · 2023Article
- Kaempferol Alleviates Mitochondrial Damage by Reducing Mitochondrial Reactive Oxygen Species Production in Lipopolysaccharide-Induced Prostate Organoids.Foods (Basel, Switzerland) · 2023Article
- Investigations into the Signaling Pathways Involving Glucose-Stimulated Zinc Secretion (GSZS) from Prostate Epithelial Cells In Vitro and In Vivo.Molecular imaging and biology · 2023Article
- Genetically elevated bioavailable testosterone level was associated with the occurrence of benign prostatic hyperplasia.Journal of endocrinological investigation · 2023Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBenign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS) are conditions extremely prevalent in the aging male. Although androgens are involved in prostate growth during developmental age, their role in the pathogenesis of BPH/LUTS is debated. Recent data indicate that low testosterone and high estradiol favor disease progression. In addition, the role of other determinants, such as metabolic syndrome or prostate inflammation, is emerging.
aimWe reviewed the evidence regarding the pathogenesis of BPH/LUTS with particular attention to metabolic influence. MATERIALS AND
methodsA review of published evidence was performed using Medline.
resultsAvailable evidence shows that a three-hit hypothesis can be drawn. An overt, or even a subclinical, bacterial or viral infection could induce prostatic inflammation (first hit) that could be autosustained or exacerbated by the presence of an altered metabolism and in particular by hypercholesterolemia (second hit). Hypogonadism and/or hyperestrogenism could act as a third hit, favoring the maintenance of this inflammatory state. The combined action of all three hits, or even two of them, may result in overexpression of Toll-like receptors (TLRs), transformation of prostatic cells into antigen-presenting cells and activation of resident human prostate-associated lymphoid tissue ending in overproduction of growth factors which, in turn, will induce prostate remodeling and further prostate enlargement. The mechanical obstruction, along with the direct action of the unfavorable metabolic and hormonal milieu on the bladder neck, helps in generating LUTS.
conclusionInflammation, dyslipidemia and altered sex-steroid milieu mutually concur in determining BPH/LUTS.
Indexed as
Identifiers
What 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.