Ketoconazole Contributes to Cryptorchidism Outcome Via Modulating Macrophage Trem2
Status:
RECRUITING
Trial end date:
2024-12-31
Target enrollment:
Participant gender:
Summary
Reduced hormone insulin-like 3, exclusively secreted by Leydig cells, has been identified as the recognized mechanism for cryptorchidism. Testicular macrophages residing in the testicular interstitium were thought to play a vital role in maintaining hormone secretion of Leydig cells. However, the contribution of macrophages to cryptorchidism remained poorly understood. Here, after 14 days of ketoconazole treatment, levels of both Trem2 and insulin-like 3 significantly decrease in human embryonic testes compared to the untreated control group. Conversely, 14 days of luteinizing hormone stimulation lead to elevated levels of Trem2 and insulin-like 3 in the testes compared to the untreated control group. Additionally, researchers find a positive correlation between Trem2 and insulin-like 3 expression in a human ex vivo tissue culture model. In summary, the study will propose Trem2 as a novel target for maintaining normal testicular descent by regulating the testicular immune microenvironment.