良性前列腺增生症（benign   prostatic   hyperplasia ，BPH）是一种常见的男性疾病，其发病基础是老年和具有功能的睾丸，但是迄今为止，其发病机制尚未完全明了。上皮间质转化（epithelial-mesenchymal  transition ，EMT）直接参与恶性肿瘤发生发展，其涉及细胞从上皮细胞向间充质细胞的转化，伴随着细胞形态的改变、细胞间相互作用的调节以及细胞的迁移和侵袭。近年来研究提示EMT是前列腺增生的一个关键过程，在前列腺增生的发生发展中起到重要作用，可以通过影响细胞的增殖、存活、衰老、代谢和免疫等生理过程，进而影响前列腺组织的生长和重构。其中，研究发现调节EMT的磷脂酰肌醇3-激酶（phosphatidylinostol  3-lcinases ，PI3K）/蛋白激酶b信号通路（AKT）和转化生长因子β信号通路（transforming   groweh   factor-β ,   TGF-β)等，可以对前列腺增生的发生发展产生重要影响。因此，深入研究EMT在前列腺增生中的作用机制，有助于发掘新的治疗靶点，本综述旨在深入探讨EMT在前列腺增生发病机制中的关键作用，着重强调细胞信号通路在良性前列腺增生EMT的机制，为未来研究和治疗提供了有益的参考和洞察，为疾病的预防和治疗提供新的思路。

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良性前列腺增生症（benign  prostatic hyperplasia， BPH）是一种常见的男性疾病，其临床表现主要为下尿路症状（lower urinary  tract  symptoms，LUTS），例如尿频和排尿困难等[1]。组织学上主要表现为前列腺间质和腺体成分的增生。该病通常会随着年龄的增长而发生，且据统计，其全球患病率逐年上升，成为男性健康领域中的重要问题之一。在不同地区和族群之间，前列腺增生的发病率存在差异。前列腺增生的发病率随着年龄的增长逐渐升高。50岁以上男性BPH患病率为50%~70%，并随着年龄的增长而增加，70岁以上BPH患病率超过80%[2]。研究表明，BPH患病率在各地有显著的差异，欧美国家的BPH患病率通常较高，尤其是在西方国家的老年男性中。相比之下，亚洲国家的患病率通常较低，特别是在东南亚地区[3]。BPH的发病率与生活方式和环境因素也有关系，研究表明，饮食结构、运动习惯、吸烟和饮酒等生活方式因素与前列腺增生的发病率相关[4]。此外，前列腺增生的发病率还与其他危险因素如高血压、糖尿病、肥胖等因素有关[5]。本综述旨在深入探讨上皮间质转化（epithelial-mesenchymal  transition ，EMT）在BPH发病机制中的关键作用。着重强调细胞信号通路在BPH中EMT的机制。

1 前列腺增生发病机制

2 上皮间质转化

3 TGF-β信号通路在BPH中作用

4 Wnt/β-catenin信号通路在BPH中作用

5 PI3K-AKT信号通路在BPH中作用

6 缺氧诱导因子-1α与 EMT 在 BPH 中的作用

众多研究发现EMT在前列腺增生中起着重要作用，其参与了BPH的发病和进展过程。因此，研究EMT在BPH中的作用，对于临床治疗和诊断具有重要意义。本文探讨了EMT在前列腺增生中的作用机制，并着重分析了TGF-β/Smad信号通路、Wnt/β-catenin和PI3K-AKT信号通路以及缺氧诱导因子在其中的作用。结论表明，EMT在前列腺增生的发生和发展中起着重要作用，不仅影响前列腺细胞的增殖和分化，还参与了前列腺组织的重塑和侵袭。缺氧环境下HIF-1α的表达与EMT各信号通路的同步激活，可能是最终导致前列腺增生的重要发病机制。因此，针对EMT相关的信号通路和分子机制的治疗策略可能会成为前列腺增生的新治疗方法。此外，EMT的生物标志物在前列腺增生的早期诊断和预后评估中也具有潜在的应用价值。尽管EMT在BPH的发病机制的标记物、信号通路以及相关蛋白有待进一步深入研究，但EMT在前列腺增生的诊治中具有广阔的应用前景，值得深入研究和探索。

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