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REVIEW article

Front. Oncol.

Sec. Cancer Molecular Targets and Therapeutics

Volume 15 - 2025 | doi: 10.3389/fonc.2025.1579539

This article is part of the Research TopicNew potential biomarkers and cellular strategies for the study of prostate cancer and testicular cancer cellsView all 8 articles

The Pathogenesis of Benign Prostatic Hyperplasia and the Roles of Prdx3, Oxidative Stress, Pyroptosis and Autophagy: A Review

Provisionally accepted
Junjie  XiangJunjie Xiang1,2Yuxuan  ZhengYuxuan Zheng3Diang  ChenDiang Chen2Yining  ZengYining Zeng4Jingqi  ZhangJingqi Zhang1Degui  ChangDegui Chang2*Cheng  ChangCheng Chang5
  • 1School of Clinical Medicine, Chengdu University of Traditional Chinses Medicine, Chengdu, Sichuan Province, China
  • 2Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan Province, China
  • 3Shool of Acupuncture and Massage, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan Province, China
  • 4Eye Hospital, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan Province, China
  • 5Jiangsu Provincial Hospital of Traditional Chinese Medicine, Nanjing, Jiangsu Province, China

The final, formatted version of the article will be published soon.

Benign prostatic hyperplasia (BPH) is driven by hormonal and inflammatory mechanisms, yet emerging factors such as peroxiredoxin 3 (Prdx3), oxidative stress (OS), pyroptosis, and autophagy remain understudied. This review synthesizes their roles in BPH pathogenesis. We demonstrate that Prdx3 inhibits autophagy, exacerbates OS, and induces pyroptosis, ultimately promoting prostate cell proliferation. Paradoxically, while Prdx3 mitigates OS, its interaction with autophagy amplifies oxidative damage. These findings challenge conventional antioxidant therapies, suggesting that enhancing antioxidant capacity may inadvertently worsen BPH progression. Our analysis provides novel insights into therapeutic strategies targeting these pathways.

Keywords: Benign prostatic hyperplasia, hormone, Inflammation, Peroxiredoxin 3, pyroptosis, Autophagy, Oxidative Stress

Received: 19 Feb 2025; Accepted: 16 Jul 2025.

Copyright: © 2025 Xiang, Zheng, Chen, Zeng, Zhang, Chang and Chang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Degui Chang, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan Province, China

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