ArticleWorld journal of urology2025
Hydroxycitric acid inhibits ferroptosis and ameliorates benign prostatic hyperplasia by upregulating the Nrf2/GPX4 pathway.
Article in World journal of urology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Lipoxin A4 improves myocardial ischemia/reperfusion injury through the Notch1-Nrf2 signaling pathway.Open life sciences · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeBenign prostatic hyperplasia (BPH) poses a significant public health challenge, affecting a substantial portion of aging men worldwide. Current therapeutic options offer limited efficacy. The pathogenesis of BPH is multifactorial, involving ferroptosis, oxidative stress, and chronic inflammation. Hydroxycitric acid (HCA) is a natural compound with diverse pharmacological activities, including the inhibition of ferroptosis, anti-inflammatory, anti-oxidative stress, and anti-tumor effects. However, its role in BPH remains unexplored. This study aimed to investigate the effects of HCA on BPH and elucidate the underlying mechanisms, with the goal of providing novel therapeutic insights for BPH treatment.
methodsC57BL/6J mice were used to establish a BPH model induced by testosterone propionate (TP). Animals were then randomly assigned to the following groups: Sham, BPH, BPH + Lip-1, BPH + Bru, BPH + HCA + Bru, and BPH + HCA. Prostate index (PI) was determined, and histopathological changes were evaluated by hematoxylin and eosin (HE) staining. Mitochondrial morphology was analyzed by TEM. The levels of Fe
resultsCompared to the Sham group, the prostate tissues of the BPH group exhibited typical histopathological features of hyperplasia, including epithelial cell proliferation, increased glandular lumen size. Concurrently, the levels of ferroptosis markers Fe
conclusionHCA inhibits ferroptosis by activating the Nrf2/GPX4 pathway, thereby ameliorating the pathological changes in BPH induced by TP. This study suggests a novel therapeutic strategy for BPH.
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