ReviewAsian journal of andrology2026
Cryptorchidism and infertility: what do we know so far?
Review in Asian journal of andrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Cryptorchidism is recognized as a significant risk factor for male germ cell tumors and infertility, with a complex and multifaceted mechanism contributing to male infertility. When the testes fail to descend into the scrotum, increased local temperature and pressure lead to increased apoptosis of spermatogenic and Sertoli cells. Additionally, disruptions in the hypothalamic-pituitary-gonadal axis result in decreased testosterone levels within the testes, and abnormal secretion of follicle-stimulating hormone and luteinizing hormone, negatively impacting spermatogenesis. Cryptorchidism also induces increased oxidative stress within the testes, leading to sperm DNA damage and impairment of the sperm plasma membrane, hindering sperm-oocyte fusion. Unilateral cryptorchidism may cause injury to the ipsilateral genitofemoral nerve, further affecting the contralateral testis by increasing oxidative stress and apoptosis. Moreover, the production of antisperm antibodies can trigger autoimmune responses, potentially damaging germ cells and contributing to infertility. Damage to type A dark spermatogonia (type Ad spermatogonia) is also considered a high-risk factor for male infertility. Understanding the mechanisms by which cryptorchidism leads to male infertility may provide new avenues for enhancing fertility in affected patients.
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