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KAT2A通过激活P38/MAPK信号通路来驱动颗粒状细胞功能障碍,从而导致过早的卵巢功能不充分

Jia Li¹, Yiting Liu¹, Linfei Huang²

¹School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang, People's Republic of China.

Biology of reproduction

|February 20, 2026

概括

氨酸乙转移酶2A (KAT2A) 在早产卵巢衰竭 (POI) 中升高. 通过p38/MAPK通路,KAT2A驱动卵巢功能障碍和衰老,这表明它是治疗点.

科学领域:

生殖生物学生殖生物学
分子内分泌学分子内分泌学
细胞衰老细胞衰老

背景情况:

过早的卵巢缺陷 (POI) 会导致不孕,卵巢功能在40岁之前就会丧失.
酸乙转移酶2A (KAT2A) 与发育,基因组稳定性和衰老有关.
目前尚不清楚KAT2A在POI发病过程中的具体作用.

研究的目的:

调查KAT2A在早产卵巢缺陷 (POI) 进展中的作用.
阐明KAT2A在POI中的功能背后的分子机制.

主要方法:

从POI患者和老鼠卵巢中获得的人类颗粒细胞 (hGCs) 中量化KAT2A表达.
评估KAT2A过度表达对小鼠生殖参数和卵巢储备的影响.
利用基因组丰富分析和p38/MAPK通路抑制进行机理学研究.

主要成果:

在POI患者和老鼠卵巢的hGC中,KAT2A的表达显著增加.
过度表达KAT2A会恶化雌激素循环,激素平衡,卵泡发育和卵巢储备,同时增加卵泡缩.
过度表达KAT2A加剧了小鼠颗粒细胞 (mGC) 中的活性氧物种 (ROS) 诱导的亡,由p38/MAPK途径介导.

结论:

KAT2A的上调与POI的发病有关.
KAT2A-p38/MAPK信号轴在KAT2A介导的卵巢功能障碍中发挥着至关重要的作用.
KAT2A代表了解决女性生殖衰老和POI的潜在治疗目标.

关键词:

氨酸乙转移酶2a (kat2a) 是一种灭症 (apoptosis) 是一种死亡的过程.颗粒状细胞是颗粒状细胞.p38/mapk信号通路的使用情况过早的卵巢功能不充分.

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