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Updated: Jan 13, 2026

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血管光滑肌细胞特异性BCAT2缺乏减轻糖尿病动脉样硬化化通过希斯 propionylation

Lili Zhang^1,2, Yujie Yang^1,2, Wei Yuan^1,2

¹Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China.

Research (Washington, D.C.)

|January 8, 2026

概括

分支链氨基酸转氨酶2 (BCAT2) 通过促进光滑肌肉细胞的骨质分化来驱动糖尿病血管化. 向BCAT2分支链α-酸 (BCKA) 途径可能为糖尿病心血管并发症提供新的治疗策略.

科学领域:

生物化学和新陈代谢
心血管研究研究心血管研究
糖尿病并发症糖尿病并发症

背景情况:

糖尿病患者因血管化而面临心血管事件风险增加.
糖尿病动脉样硬化化的精确治疗目标仍然难以捉摸.
分支链氨基酸转氨酶2 (BCAT2),参与分支链氨基酸 (BCAA) 代谢,是糖尿病并发症的潜在因素.

研究的目的:

调查BCAT2在糖尿病动脉样硬化化的发展中的作用.
阐明BCAT2对糖尿病血管化贡献的基础分子机制.

主要方法:

使用空气流辅助脱电喷射电离化质谱成像 (AFADESI-MSI) 进行糖尿病脚截肢动脉部分的空间代谢物分析.
分析了单细胞RNA测序数据集,以识别糖尿病动脉中的BCAA代谢酶表达.
生成的ApoE淘汰赛小鼠具有血管光滑肌细胞 (VSMC) 特定的BCAT2删除,以模拟糖尿病动脉样硬化化.

主要成果:

空间代谢学揭示了糖尿病患者化动脉中增强的BCAA代谢.
单细胞转录组学在加糖尿病动脉的VSMC中发现了上调的BCAT2.
特定于VSMC的BCAT2缺陷显著降低了糖尿病动脉样硬化化,并补充了分支链α-酸 (BCKA),促进了VSMC的骨质分化.

结论:

在糖尿病动脉样硬化化中发现了BCAA代谢,特别是BCAT2-BCKA轴的新型作用.
证明BCAT2通过通过基因组 propionylation通过表观遗传调节RUNX2促进VSMC骨质细胞分化.
确定了BCAT2-BCKA通路作为减轻糖尿病血管化的潜在治疗标.

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