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内皮JMJD1C通过激活SREBF2-依赖胆固醇生物合成来驱动病态的眼球新血管化

Yang Yu¹, Zhangyu Liu², Jiayu Huang²

¹the Affiliated Eye Hospital, Nanjing Medical University, Nanjing, China; The Fourth School of Clinical Medicine, Nanjing Medical University, Nanjing, China; Department of Ophthalmology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.

Free radical biology & medicine

|January 18, 2026

概括

组织素脱甲基酶JMJD1C通过调节内皮胆固醇合成来驱动病态眼球血管生成. 抑制JMJD1C为眼睛血管疾病提供了潜在的治疗策略.

科学领域:

眼科医生眼科眼科
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

病态的眼部新血管化与异常的组织蛋白修饰有关.
驱动这些变化的精确分子机制尚未完全理解.
这项研究的重点是基因组脱甲基酶JMJD1C及其在病态血管生成中的作用.

研究的目的:

研究JMJD1C在病态眼球血管生成中的功能.
评估JMJD1C作为眼血管疾病的治疗点.

主要方法:

在小鼠模型和内皮细胞 (ECs) 中使用分子技术检查了Jmjd1c表达.
在体外和体内对JMJD1C的益血管功能进行了评估.
使用RNA测序,ChIP-qPCR和其他测试剖析分子机制.

主要成果:

在OIR和CNV模型中,内皮特异性的Jmjd1c删除显著降低了新血管化.
JMJD1C的丧失影响了EC的扩散,迁移,管状形成和发芽.
删除Jmjd1c通过H3K9me2标记抑制了Srebf2转录和胆固醇生物合成.
药理上的JMJD1C抑制也减少了新血管化.

结论:

JMJD1C是病态眼血管新生的一个关键调节器.
它通过基因组脱甲基化控制内皮胆固醇生物合成.
JMJD1C-Srebf2轴是眼血管疾病的潜在治疗标.

关键词:

希斯甲基化希斯甲基化在 JMJD1C 里面.在SREBF2中,胆固醇的生物合成病理性血管新生病理性血管新生.

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