睾丸源性生殖障碍综合征研究进展

Testicular dysgenesis syndrome:An update

睾丸源性生殖障碍综合征(TDS)是近10年来男性不育领域研究的热点。环境内分泌干扰因子作用于睾丸Leydig细胞和/或Sertoli细胞致使睾丸发育异常,从而导致TDS症状的出现是被广泛接受的发病机制。分子生物学研究提示类胰岛素样因子3(INSL-3)、雄激素受体(AR)、P27kip蛋白、WT-1基因及副中肾管抑制物(M IS)等可能与TDS的发病有关,本文对TDS的病因、机制及研究进展等进行了综述。

Researches on the testicular dysgenesis syndrome（TDS） have flourished in the recent decade,and a widely accepted view on its pathogenesis is that environmental endocrine disrupting chemicals（EDCs） act on Leydig cells and/or testicular Sertoli cells,resulting in abnormal development of the testis and leading to the symptoms of TDS.Molecular biological studies suggest a correlation of TDS etiology with insulin-like factor 3（INSL-3）,androgen receptor（AR）,P27kip,WT-1 and Müllerian inhibiting substance（MIS）.This review focuses on the progress in current researches on the etiology and mechanism of TDS.