Androgens and estrogens in benign prostatic hyperplasia: past, present and future.
Androgens and estrogens in benign prostatic hyperplasia: past, present and future.
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良性前列腺增生的雄激素和雌激素：过去，现在和未来。
DOI：
10.1016/j.diff.2011.04.006
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发表时间：
2011-11
期刊：
影响因子：
2.9
通讯作者：
Ricke, William A.
中科院分区：
文献类型：
--
作者：
Nicholson, Tristan M.;Ricke, William A.
良性前列腺增生（BPH）及相关下尿路症状（LUTS）是泌尿外科常见的临床问题。虽然确切的分子病因尚不清楚，但性类固醇与BPH的发展和维持有关。有足够的数据表明雄激素和雄激素受体途径与前列腺增生有关，使用雄激素还原化合物，如阻断睾酮向二氢睾酮转化的5α-还原酶抑制剂，是前列腺肥大导致LUTS患者标准护理的一个组成部分。然而，前列腺增生是一种多因素疾病，并不是所有男性对目前可用的治疗都有良好的反应，这表明除雄激素外的其他因素也参与其中。睾酮是男性的主要循环雄激素，也可以通过CYP19/芳香化酶代谢为强效雌激素雌二醇-17β。前列腺是雌激素的靶组织，雌激素直接或间接影响前列腺的生长和分化。内源性和外源性雌激素在BPH中直接影响前列腺生长和分化的确切作用是一个尚未充分研究的领域。雌激素和选择性雌激素受体调节剂（SERMs）已被证明可促进或抑制前列腺增生，这表明其在前列腺增生中的潜在作用。最近的研究表明，雌激素受体信号通路可能在BPH和LUTS的发展和维持中起重要作用；然而，需要新的模型来从遗传学角度剖析雌激素调控的BPH分子机制。为了通过膳食和治疗性serm靶向BPH，需要更多的工作来确定BPH中的雌激素和相关信号通路。
Benign prostatic hyperplasia (BPH) and associated lower urinary tract symptoms (LUTS) are common clinical problems in urology. While the precise molecular etiology remains unclear, sex steroids have been implicated in the development and maintenance of BPH. Sufficient data exists linking androgens and androgen receptor pathways to BPH and use of androgen reducing compounds, such as 5α-reductase inhibitors which block the conversion of testosterone into dihydrotestosterone, are a component of the standard of care for men with LUTS attributed to an enlarged prostate. However, BPH is a multifactorial disease and not all men respond well to currently available treatments, suggesting factors other than androgens are involved. Testosterone, the primary circulating androgen in men, can also be metabolized via CYP19/aromatase into the potent estrogen, estradiol-17β. The prostate is an estrogen target tissue and estrogens directly and indirectly affect growth and differentiation of prostate. The precise role of endogenous and exogenous estrogens in directly affecting prostate growth and differentiation in the context of BPH is an understudied area. Estrogens and selective estrogen receptor modulators (SERMs) have been shown to promote or inhibit prostate proliferation signifying potential roles in BPH. Recent research has demonstrated that estrogen receptor signaling pathways may be important in the development and maintenance of BPH and LUTS; however, new models are needed to genetically dissect estrogen regulated molecular mechanisms involved in BPH. More work is needed to identify estrogens and associated signaling pathways in BPH in order to target BPH with dietary and therapeutic SERMs.
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