ArticleScientific reports2023
High glucose promotes benign prostatic hyperplasia by downregulating PDK4 expression.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Integrating single-cell and bulk transcriptomic analyses to explore key lactylation-related genes in benign prostatic hyperplasia.Scientific reports · 2026Article
- A bioinformatics analysis of the PIEZO channel interaction network and the genes related to glycometabolic reprogramming and mitochondrial oxidative phosphorylation in the progression of prostatic hyperplasia.Translational andrology and urology · 2026Article
- Investigating the impact of gut microbiota-derived metabolites on benign prostatic hyperplasia using network pharmacology approaches.BMC pharmacology & toxicology · 2026Article
- Endoplasmic reticulum-mitochondria contact sites in benign prostatic hyperplasia: evidence integration and mechanistic hypotheses.Frontiers in immunology · 2026Review
- Identification and validation of genes associated with mitochondria in cerebral infarction and benign prostatic hyperplasia.Frontiers in medicine · 2026Article
- A retrospective cohort study on the improvement of urodynamic parameters and NIH-CPSI scores with Relin granules in BPH patients with high prostatitis-like symptom scores.American journal of translational research · 2026Article
- Predicting benign prostatic hyperplasia risks: model development and external validation based on three cohorts.Global health research and policy · 2025Article
- Midline-1 inhibited high glucose-induced epithelial-mesenchymal transition, fibrosis and inflammation through WNT/β-catenin signaling in benign prostatic hyperplasia.Frontiers in endocrinology · 2025Article
- Proteomic Analysis of the Effects of Shenzhu Tiaopi Granules on Model Rats with Type 2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Genetic Ablation of Pyruvate Dehydrogenase Kinase Isoform 4 Gene Enhances Recovery from Hyperoxic Lung Injury: Insights into Antioxidant and Inflammatory Mechanisms.Biomedicines · 2024Article
- Identification and functional activity of Nik related kinase (NRK) in benign hyperplastic prostate.Journal of translational medicine · 2024Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As men age, a growing number develop benign prostatic hyperplasia (BPH). According to previous research, diabetes may be a risk factor. Pyruvate dehydrogenase kinase 4 (PDK4) is closely related to glucose metabolism and plays a role in the onset and progression of numerous illnesses. This study aimed to determine the direct effects of high glucose environment on prostate epithelial cells, in particular by altering PDK4 expression levels. In this investigation, normal prostatic epithelial cells (RWPE-1) and human benign prostatic hyperplasia epithelial cells (BPH-1) were treated with 50 mM glucose to show the alteration of high glucose in prostate cells. PDK4-target siRNA, PDK4-expression plasmid were used to investigate the effects of PDK4. Rosiglitazone (RG), a PPARγ agonist, with the potential to up-regulate PDK4 expression was also used for treating prostate cells. The expression of PDK4 in human prostate samples was also analyzed. The effects of high glucose therapy on BPH-1 and RWPE-1 cells were demonstrated to enhance proliferation, epithelial-mesenchymal transition (EMT), suppress apoptosis, and down-regulate PDK4 expression. Additionally, diabetes-related BPH patients had reduced PDK4 expression. Following the application of PDK4-target siRNA, a comparable outcome was seen. The PDK4-expression plasmid therapy, however, produced the opposite results. RG with the ability to elevate PDK4 expression might be used to treat BPH. Changes in the metabolism of lipids and glucose may be the cause of these consequences. These findings showed that high glucose treatment might facilitate BPH development, and may be related to the down-regulation of PDK4. PDK4 might be a potential therapeutic target of BPH.
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