ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2024
Aging-Related Mitochondrial Dysfunction Is Associated With Fibrosis in Benign Prostatic Hyperplasia.
Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- Mitochondrial dysfunction in urologic disease.Prostate cancer and prostatic diseases · 2026Review
- High-Throughput Proteomic and Glycoproteomic Analyses in Benign Prostatic Hyperplasia.Journal of the American Society for Mass Spectrometry · 2026Article
- Targeting fibrosis in the treatment of lower urinary tract dysfunction.The Journal of pathology · 2026Article
- Identification and validation of genes associated with mitochondria in cerebral infarction and benign prostatic hyperplasia.Frontiers in medicine · 2026Article
- ZC3H4, a novel regulator of mitochondrial complex I, impacts prostate stromal cell senescence, attachment, adhesion and anoikis resistance.Cell death & disease · 2025Article
- Defining aging-associated factors that increase susceptibility to prostate cancer.Endocrine-related cancer · 2025Review
- MSIght: A Modular Platform for Improved Confidence in Global, Untargeted Mass Spectrometry Imaging Annotation.Journal of proteome research · 2025Article
- The Importance of Mitochondrial Processes in the Maturation and Acquisition of Competences of Oocytes and Embryo Culture.International journal of molecular sciences · 2025Review
- Mechanisms of prostatic inflammation-mediated male lower urinary tract symptoms.American journal of clinical and experimental urology · 2025Review
- Unveiling therapeutic targets and preventive components for kidney insufficiency and blood stasis-type BPH: bridging metabolomics, network pharmacology and reverse screening.Frontiers in pharmacology · 2025Article
- Article
- Increased Risk of Benign Prostate Hyperplasia (BPH) in Patients with Gout: A Longitudinal Follow-Up Study Using a National Health Screening Cohort.Diagnostics (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAge is the greatest risk factor for lower urinary tract symptoms attributed to benign prostatic hyperplasia (LUTS/BPH). Although LUTS/BPH can be managed with pharmacotherapy, treatment failure has been putatively attributed to numerous pathological features of BPH (eg, prostatic fibrosis, inflammation). Mitochondrial dysfunction is a hallmark of aging; however, its impact on the pathological features of BPH remains unknown.
methodsPublicly available gene array data were analyzed. Immunohistochemistry examined mitochondrial proteins in the human prostate. The effect of complex I inhibition (rotenone) on a prostatic cell line was examined using quantitative polymerase chain reaction, immunocytochemistry, and Seahorse assays. Oleic acid (OA) was tested as a bypass of complex I inhibition. Aged mice were treated with OA to examine its effects on urinary dysfunction. Voiding was assessed longitudinally, and a critical complex I protein measured.
resultsMitochondrial function and fibrosis genes were altered in BPH. Essential mitochondrial proteins (ie, voltage-dependent anion channels 1 and 2, PTEN-induced kinase 1, and NADH dehydrogenase [ubiquinone] iron-sulfur protein 3, mitochondrial [NDUFS3]) were significantly (p < .05) decreased in BPH. Complex I inhibition in cultured cells resulted in decreased respiration, altered NDUFS3 expression, increased collagen deposition, and gene expression. OA ameliorated these effects. OA-treated aged mice had significantly (p < .05) improved voiding function and higher prostatic NDUFS3 expression.
conclusionsComplex I dysfunction is a potential contributor to fibrosis and lower urinary tract dysfunction in aged mice. OA partially bypasses complex I inhibition and therefore should be further investigated as a mitochondrial modulator for treatment of LUTS/BPH. Hypotheses generated in this investigation offer a heretofore unexplored cellular target of interest for the management of LUTS/BPH.
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