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Disruption of estrogen receptor signaling and similar pathways in the efferent ductules and initial segment of the epididymis

机译：雌激素受体信号和中断传出微胆管和类似的途径附睾的初始段

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Seminiferous tubular atrophy may involve indirectly the disruption of estrogen receptor-a (ESR1) function in efferent ductules of the testis. ESR1 helps to maintain fluid resorption by the ductal epithelium and the inhibition or stimulation of this activity in rodent species will lead to fluid accumulation in the lumen. If not resolved, the abnormal buildup of fluid in the head of the epididymis and efferent ductules becomes a serious problem for the testis, as it leads to an increase in testis weight, tubular dilation and seminiferous epithelial degeneration, as well as testicular atrophy. The same sequence of pathogenesis occurs if the efferent ductule lumen becomes occluded. This review provides an introduction to the role of estrogen in the malereproductive tract but focuses on the various overlapping mechanisms that could induce efferent ductule dysfunction and fluid backpressure histopathology. Although efferent ductules are difficult to find, their inclusion in routine histological evaluations is recommended, as morphological images of these delicate tubules may be essential for understanding the mechanism of testicular injury, especially if dilations are observed in the rete testis and/or seminiferous tubules.Signature Lesion:The rete testis and efferent ductules can appear dilated, as if the lumens were greatly expanded with excess fluid or the accumulation of sperm. Because the efferent ductules resorb most of the fluid arriving from the rete testis lumen;one of two mechanisms is likely to be involved: a) reduced fluid uptake, which has been caused by the disruption in estrogen receptor signaling or associated pathways; or b) an increased rate of fluid resorption, which results in luminal occlusion. Bothmechanisms can lead to a temporary increase in testicular weight, tubular dilation and atrophy of the seminiferous tubules.
机译：细精管状萎缩可能涉及间接雌激素受体的破坏(ESR1)传出微胆管的函数睾丸。导管上皮细胞和抑制在啮齿动物物种刺激的活动将导致腔积液。不解决,异常体液聚积附睾的负责人和传出微胆管为睾丸,变成了一个严重的问题导致睾丸重量的增加,管状扩张和精上皮变性,以及睾丸萎缩。发病机理发生如果序列相同传出小导管腔变得闭塞。审查提供了一个介绍的角色雌激素在malereproductive束关注各种重叠的机制可能诱发传出小导管功能障碍和流体反压力组织病理学。传出微胆管很难找到他们包含在常规组织学评价这些建议,形态学图像精致的小管可能是必不可少的了解睾丸损伤的机制,特别是如果膨胀包括观察膜层睾丸和/或细精管。病变:睾丸网和传出微胆管出现扩张,如果流明扩大液体或过剩的积累精子。从睾丸网液到达腔,两种机制之一可能是涉及:1)减少液体吸收,一直雌激素受体的破坏造成的信号或相关的通路;增加流体的速度吸收,这结果在腔的阻塞。临时增加睾丸重量,精管扩张和萎缩小管。

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