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睾丸发育不全综合征:机制见解及潜在的新下游效应

Testicular dysgenesis syndrome: mechanistic insights and potential new downstream effects.

作者信息

Sharpe Richard M, Skakkebaek Niels E

机构信息

MRC Human Reproductive Sciences Unit, Centre for Reproductive Biology, The Queen's Medical Research Institute, Edinburgh, United Kingdom.

出版信息

Fertil Steril. 2008 Feb;89(2 Suppl):e33-8. doi: 10.1016/j.fertnstert.2007.12.026.

Abstract

Reproductive disorders of newborn (cryptorchidism, hypospadias) and young adult males (low sperm counts, testicular germ cell cancer) are common and/or increasing in incidence. It has been hypothesized that these disorders may comprise a testicular dysgenesis syndrome (TDS) with a common origin in fetal life. This has been supported by findings in an animal model of TDS involving fetal exposure to n(dibutyl) phthalate, as well as by new clinical studies. Recent advances in understanding from such studies have led to refinement of the TDS hypothesis, highlighting the central role that deficient androgen production/action during fetal testis development, may play in the origin of downstream disorders.

摘要

新生儿(隐睾症、尿道下裂)和年轻成年男性(精子数量低、睾丸生殖细胞癌)的生殖系统疾病很常见,且发病率正在上升。据推测,这些疾病可能构成一种睾丸发育不全综合征(TDS),其起源于胎儿期。这一推测得到了TDS动物模型研究结果的支持,该模型涉及胎儿暴露于邻苯二甲酸二丁酯,同时也得到了新的临床研究的支持。这些研究在认识上的最新进展使得TDS假说得到了完善,强调了胎儿睾丸发育过程中雄激素生成/作用不足在下游疾病起源中可能发挥的核心作用。

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