Testicular dysgenesis syndrome: mechanistic insights and potential new downstream effects.
Testicular dysgenesis syndrome: mechanistic insights and potential new downstream effects.
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DOI：
10.1016/j.fertnstert.2007.12.026
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发表时间：
2008-02-01
影响因子：
6.7
通讯作者：
Skakkebaek, Niels E
中科院分区：
文献类型：
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作者：
Sharpe, Richard M;Skakkebaek, Niels E
新生儿（隐睾、尿道下裂）和年轻成年男性（精子数量低、睾丸生殖细胞癌）的生殖障碍很常见，发病率也在增加。据推测，这些疾病可能包括睾丸发育不良综合征（TDS）与胎儿生活的共同起源。在涉及胎儿暴露于邻苯二甲酸二丁酯的TDS动物模型中的发现，以及新的临床研究，都支持了这一点。这些研究的最新进展使TDS假说得到了完善，强调了胎儿睾丸发育过程中雄激素产生/作用不足可能在下游疾病的起源中发挥的核心作用。
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.