Mechlin Clay, Kogan Barry
Albany Medical College.
Transl Androl Urol. 2012 Jun;1(2):97-102. doi: 10.3978/j.issn.2223-4683.2012.06.03.
If untreated, cryptorchidism leads to age dependent decreases in germ cell number (GCN) and testicular fibrosis. The pathophysiology of this process and its long-term effects on fertility are unclear. Mast cells are intricately involved in inflammation and fibrosis in a variety of organ systems. Their secretory products have mitogenic effects on fibroblasts and promote collagen deposition. Mast cell activation and migration are under the influence of estrogens and this interaction has been demonstrated in the testes in several animal models. Models of cryptorchidism have shown increased estrogen levels and expression of estrogen receptors in undescended testes compared to controls. Mast cell numbers have positively correlated with testicular fibrosis in human studies and decreased spermatogenesis as well. We found no human studies of mast cells in cryptorchid testes. However several animal models have investigated the effect of estrogens on mast cells and spermatogenesis in undescended testes. In this review we examine the possible links between estrogens, mast cells, and testicular fibrosis in cryptorchidism, focusing on histological studies.
如果不进行治疗，隐睾症会导致生殖细胞数量（GCN）随年龄增长而减少以及睾丸纤维化。这一过程的病理生理学及其对生育能力的长期影响尚不清楚。肥大细胞复杂地参与多种器官系统的炎症和纤维化过程。它们的分泌产物对成纤维细胞有促有丝分裂作用，并促进胶原蛋白沉积。肥大细胞的激活和迁移受雌激素影响，这种相互作用已在多种动物模型的睾丸中得到证实。与对照组相比，隐睾症模型显示未降入阴囊的睾丸中雌激素水平升高且雌激素受体表达增加。在人体研究中，肥大细胞数量与睾丸纤维化呈正相关，同时也与精子发生减少有关。我们未发现有关隐睾症睾丸中肥大细胞的人体研究。然而，一些动物模型已经研究了雌激素对未降入阴囊睾丸中肥大细胞和精子发生的影响。在本综述中，我们将重点关注组织学研究，探讨雌激素、肥大细胞和隐睾症中睾丸纤维化之间的可能联系。
