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通过单细胞转录组谱分析解码隐睾症中精子发生失败的发病机制。

Decoding the pathogenesis of spermatogenic failure in cryptorchidism through single-cell transcriptomic profiling.

机构信息

Key Laboratory of Organ Regeneration and Reconstruction, State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China; Beijing Institute for Stem Cell and Regenerative Medicine, Beijing, China.

State Key Laboratory of Female Fertility Promotion, Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, China.

出版信息

Cell Rep Med. 2024 Sep 17;5(9):101709. doi: 10.1016/j.xcrm.2024.101709. Epub 2024 Sep 2.

Abstract

Cryptorchidism, commonly known as undescended testis, affects 1%-9% of male newborns, posing infertility and testis tumor risks. Despite its prevalence, the detailed pathophysiology underlying male infertility within cryptorchidism remains unclear. Here, we profile and analyze 46,644 single-cell transcriptomes from individual testicular cells obtained from adult males diagnosed with cryptorchidism and healthy controls. Spermatogenesis compromise in cryptorchidism links primarily to spermatogonium self-renewal and differentiation dysfunctions. We illuminate the involvement of testicular somatic cells, including immune cells, thereby unveiling the activation and degranulation of mast cells in cryptorchidism. Mast cells are identified as contributors to interstitial fibrosis via transforming growth factor β1 (TGF-β1) and cathepsin G secretion. Furthermore, significantly increased levels of secretory proteins indicate mast cell activation and testicular fibrosis in the seminal plasma of individuals with cryptorchidism compared to controls. These insights serve as valuable translational references, enriching our comprehension of testicular pathogenesis and informing more precise diagnosis and targeted therapeutic strategies for cryptorchidism.

摘要

隐睾症,俗称睾丸未降,影响 1%-9%的男性新生儿,存在不育和睾丸肿瘤风险。尽管其发病率较高,但隐睾症导致男性不育的详细病理生理学机制仍不清楚。在这里,我们对来自诊断为隐睾症的成年男性和健康对照个体的睾丸细胞的 46644 个单细胞转录组进行了分析和分析。隐睾症中精子发生的损伤主要与精原细胞自我更新和分化功能障碍有关。我们揭示了睾丸体细胞(包括免疫细胞)的参与,从而揭示了隐睾症中肥大细胞的激活和脱颗粒作用。肥大细胞通过转化生长因子 β1 (TGF-β1) 和组织蛋白酶 G 的分泌被鉴定为间质纤维化的贡献者。此外,与对照组相比,隐睾症个体的精液中显著增加的分泌蛋白水平表明肥大细胞的激活和睾丸纤维化。这些研究结果为理解睾丸发病机制提供了有价值的转化参考,并为隐睾症的更精确诊断和靶向治疗策略提供了信息。

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