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在动脉样硬化中,PRDM16控制了光滑肌肉细胞的命运

Josephine M E Tan^1,2, Lan Cheng^1,2, Ryan P Calhoun^1,2

¹Institute for Diabetes, Obesity & Metabolism; Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

bioRxiv : the preprint server for biology

|March 3, 2025

概括

PRDM16保持了血管光滑肌肉细胞 (SMC) 的身份. 失去PRDM16促进SMC合成程序,驱动纤维增殖性斑块并影响心血管疾病的进展.

科学领域:

心血管生物学心血管生物学
细胞和分子医学是细胞和分子医学.

背景情况:

血管光滑肌细胞 (SMCs) 可以在应对疾病刺激时切换表型.
现型调节的SMC是动脉样硬化和心血管事件的关键.

研究的目的:

研究转录因子PRDM16在SMC身份和动脉样硬化中的作用.

主要方法:

在人类和小鼠动脉样硬化模型中研究PRDM16表达.
使用了SMC特定的淘汰赛小鼠,缺乏PRDM16.
进行单细胞分析和染色体结合测定.

主要成果:

在动脉样硬化SMC中,PRDM16的下调.
失去PRDM16会激活SMC的合成程序,即使是在恒温的条件下.
特定于SMC的PRDM16缺乏导致纤维增殖,富含原蛋白的斑块与厚厚的纤维盖.

结论:

PRDM16对于保持SMC身份至关重要.
通过抑制合成SMC程序,PRDM16作为动脉样硬化病变组成的关键决定因素.

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