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慢性全身性炎症在良性前列腺增生发病中的机制
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Abstract:
这篇综述探讨了慢性全身性炎症在良性前列腺增生发病机制中的作用，良性前列腺增生是一种常见于老年男性的疾病，可导致下尿路症状(LUTS)，严重影响中老年人的生活质量。虽然前列腺增生通常与衰老和激素变化有关，但越来越多的证据表明，由肥胖和代谢综合征等疾病引起的慢性全身性炎症是疾病进展的关键因素。以白细胞介素-6 (IL-6)和肿瘤坏死因子-α (TNF-α)等促炎标志物升高为特征的慢性全身性炎症，促进前列腺细胞增殖和组织重塑，导致前列腺增大。本综述强调了系统性炎症影响前列腺组织的机制，包括NF-κB和MAPK等关键信号通路的激活。我们还回顾了临床证据，表明系统性炎症标记物，如C-反应蛋白(CRP)和白细胞计数，与前列腺体积增加和前列腺增生患者更严重的LUTS之间有很强的相关性。本综述强调了，在BPH治疗中需要针对全身炎症，特别是对于患有严重炎症的代谢性疾病的患者。治疗前列腺增生的全身性炎症可能会有更好的改善及治疗效果。总之，通过抗炎药、他汀类药物和其他调节特定炎症通路的药物等疗法靶向全身炎症可能为减缓BPH进展和缓解症状提供有希望的解决方案。未来的研究应集中于完善这些治疗方法，并调查其长期疗效和安全性，特别是在炎症驱动的前列腺增生患者中。
This review explores the role of chronic systemic inflammation in the pathogenesis of benign prostatic hyperplasia (BPH), a condition common in aging men that leads to lower urinary tract symptoms (LUTS). While BPH is often associated with aging and hormonal changes, increasing evidence suggests that systemic inflammation, driven by conditions like obesity and metabolic syndrome, is a key factor in disease progression. Chronic systemic inflammation, characterized by elevated pro-inflammatory markers such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), promotes prostatic cell proliferation and tissue remodeling, contributing to prostate enlargement. This review highlights the mechanisms by which systemic inflammation influences prostate tissue, including the activation of critical signaling pathways like NF-κB and MAPK. We also review clinical evidence showing a strong association between systemic inflammatory markers, such as C-reactive protein (CRP) and white blood cell count, with increased prostate volume and more severe LUTS in BPH patients. The purpose of this review is to emphasize the need to target systemic inflammation in BPH management, particularly for patients with metabolic conditions that exacerbate inflammation. Addressing this aspect of BPH could lead to more effective therapies and improved outcomes for patients. In conclusion, targeting systemic inflammation through therapies like anti-inflammatory drugs, statins, and other agents that modulate specific inflammatory pathways may offer promising solutions for slowing BPH progression and alleviating symptoms. Future research should focus on refining these treatments and investigating their long-term efficacy and safety, especially in patients with inflammation-driven BPH.
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