基因素乙转移酶1通过调节单细胞基因素糖化调节促进了发作后的炎症反应
Yutong Guo1,2, Jie Xiong1, Zhaoyue Li1,3
1Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Nature communications
|November 28, 2025
概括
基因组酸化,特别是基因组H3K23succ,在心肌梗塞 (MI) 后的单细胞中被上调. 基酸转移酶1 (Hat1) 驱动这种修饰,促进炎症和恶化心脏结果在MI.
科学领域:
- 生物化学 生物化学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 心血管生物学 心血管生物学
背景情况:
- 单细胞和巨细胞的激活对于心肌梗塞 (MI) 恢复和炎症至关重要.
- 组织基因糖结合在心脏病发作期间调节单细胞表型中的作用尚不清楚.
研究的目的:
- 为了研究基因素化在MI后单细胞调节中的作用和机制.
- 确定MI期间参与基因素化中的关键酶,并评估它们的治疗潜力.
主要方法:
- 从MI患者和小鼠模型中的单细胞中分析了基因组糖化水平.
- 研究了作为顺转移酶的基因素乙转移酶1 (Hat1) 的酶活性.
- 评估了Hat1缺乏对心脏功能和炎症在MI小鼠模型的影响.
主要成果:
- 基因组糖结合,特别是H3K23succ,在心脏病患者和雄性小鼠的单细胞中升高,与炎症相关.
- 基因素乙转移酶1 (Hat1) 被确定为一种在促炎单细胞中升调的糖转移酶.
- 哈特1缺乏改善了心脏功能,减少了心脏病发作的大小,并抑制了心脏病发作后的炎症.
结论:
- 基因组酸化在早期的MI进展中发挥着关键作用,通过调节单细胞和巨细胞的表型.
- 哈特1作为表观遗传调节剂,通过H3K23化促进促炎性单细胞转化.
- 向Hat1为治疗心肌梗塞提供了治疗潜力.
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