Oxidative Stress in Benign Prostatic Hyperplasia: Mechanisms, Clinical Relevance and Therapeutic Perspectives.

IF 2.9 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
Aris Kaltsas, Timoleon Giannakas, Marios Stavropoulos, Zisis Kratiras, Michael Chrisofos
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引用次数: 0

Abstract

Background/objectives: Benign prostatic hyperplasia (BPH) is among the most common conditions affecting men as they age, resulting in lower urinary tract symptoms (LUTS) that can profoundly impact quality of life. While historically attributed primarily to androgenic imbalances, current evidence implicates additional factors-particularly oxidative stress (OS) and chronic inflammation-in BPH pathogenesis. This review aims to synthesize research on the interplay between OS, inflammation, and hormonal regulation in BPH, emphasizing their clinical relevance and potential therapeutic implications.

Methods: A comprehensive review of peer-reviewed literature was conducted focusing on mechanistic studies, clinical trials, and observational reports. Searches included data on ROS generation, antioxidant capacity, inflammatory mediators, and their contribution to pathological prostatic overgrowth. Potential interventions targeting OS-such as antioxidant supplementation, anti-inflammatory drugs, vitamin D receptor agonists, and phytotherapeutics-were also evaluated for their efficacy and safety profiles.

Results: Chronic inflammation and OS were consistently identified within hyperplastic prostate tissue. Excessive ROS production, diminished antioxidant defense, and sustained cytokine release create a proproliferative and antiapoptotic environment, accelerating disease progression. Metabolic comorbidities (e.g., obesity, insulin resistance) further exacerbate these imbalances. Standard therapies (α-blockers and 5-ARIs) effectively relieve symptoms but do not directly address the oxidative-inflammatory axis. Emerging evidence suggests that pharmacological and dietary approaches targeting OS and inflammation may reduce prostate volume expansion and alleviate LUTS.

Conclusions: Findings indicate that OS and inflammation are key contributors to BPH progression. Incorporating antioxidant and anti-inflammatory strategies alongside conventional treatments holds promise for improving clinical outcomes and patient quality of life. Future research should focus on validating OS-specific biomarkers and optimizing personalized therapy regimens.

氧化应激在良性前列腺增生:机制,临床相关性和治疗前景。
背景/目的:随着年龄的增长,良性前列腺增生(BPH)是影响男性最常见的疾病之一,导致下尿路症状(LUTS),可以深刻影响生活质量。虽然历史上主要归因于雄激素失衡,但目前的证据表明,BPH的发病机制中还有其他因素,特别是氧化应激(OS)和慢性炎症。本文综述了BPH中OS、炎症和激素调节之间相互作用的研究,强调了它们的临床意义和潜在的治疗意义。方法:对同行评议的文献进行全面回顾,重点是机制研究、临床试验和观察性报告。搜索包括ROS生成,抗氧化能力,炎症介质及其对病理性前列腺过度生长的贡献的数据。针对os的潜在干预措施,如抗氧化剂补充、抗炎药物、维生素D受体激动剂和植物疗法,也对其有效性和安全性进行了评估。结果:慢性炎症和OS在增生性前列腺组织中一致存在。过量的ROS产生、抗氧化防御减弱和持续的细胞因子释放创造了促增殖和抗凋亡的环境,加速了疾病的进展。代谢合并症(如肥胖、胰岛素抵抗)进一步加剧了这些不平衡。标准疗法(α-阻滞剂和5-ARIs)能有效缓解症状,但不能直接治疗氧化-炎症轴。新出现的证据表明,针对OS和炎症的药物和饮食方法可能会减少前列腺体积扩张并减轻LUTS。结论:研究结果表明,OS和炎症是BPH进展的关键因素。将抗氧化和抗炎策略与常规治疗相结合,有望改善临床结果和患者的生活质量。未来的研究应侧重于验证os特异性生物标志物和优化个性化治疗方案。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
0.80
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