单细胞,空间和大量转录组数据分析显示,LINC00467介导的塞尔托利细胞铁是一个潜在的治疗点和亚精子症的生物标志物
Hao Bo1, Fang Zhu2, Xueheng Zhao2
1NHC Key Laboratory of Human Stem Cell and Reproductive Engineering, Institute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, Hunan, China; Clinical Research Center for Reproduction and Genetics in Hunan Province, Reproductive and Genetic Hospital of CITIC-Xiangya, Changsha, Hunan, China.
Free radical biology & medicine
|September 2, 2025
概括
在非阻塞性精症 (NOA) 中,一种编程细胞死亡的类型 - - 铁死增加. 通过LINC00467调节的Sertoli细胞中的化可能会改善男性生育能力.
科学领域:
- 生殖生物学
- 细胞死亡机制
- 分子遗传学
背景情况:
- 精子生成涉及编程细胞死亡, 但特定类型在人类生育中的作用尚不清楚.
- 非阻塞性精症 (NOA) 是男性不孕症的主要原因,通常与丸功能障碍有关.
研究的目的:
- 调查铁死在人类精子生成和NOA中的作用.
- 确定与NOA相关的塞尔托利细胞中的关键铁细胞调节剂.
- 评估LINC00467作为NOA患者精子获取的生物标志物.
主要方法:
- 单细胞,大量RNA和空间转录组数据的综合分析.
- 权重基因共同表达网络分析 (WGCNA) 和相关性分析.
- 在体外实验和定量实时聚合酶链反应 (qRT-PCR).
主要成果:
- 在人类的精子生成中,铁亡信号升高,在丸样本中显著增加.
- 塞尔托利细胞中的GPX4依赖性铁是NOA的标志,其抑制改善了塞尔托利细胞的功能.
- 长非编码RNA (lncRNA) LINC00467被确定为塞尔托利细胞中铁亡的关键调节剂.
- 在NOA患者中,LINC00467水平与精子检索结果相关.
结论:
- 在塞尔托利细胞中增加的铁死是导致NOA的新机制.
- LINC00467是预测精子获取成功的潜在生物标志物,也是NOA的治疗点.
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