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在动脉样硬化中,血管光滑肌肉细胞的代谢重编程和表型重塑

Zhenyue Fu¹, Shuo Yang¹, Xindi Chang¹

¹Department of Cardiology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Cell death discovery

|December 30, 2025

概括

血管光滑肌细胞 (VSMC) 中的代谢重编程驱动动动脉硬化斑块的不稳定性. 针对这些代谢变化提供了稳定斑块和减缓疾病进展的新策略.

科学领域:

心血管生物学心血管生物学
代谢调节代谢调节代谢调节代谢调节
动脉样硬化研究动脉样硬化研究

背景情况:

血管光滑肌细胞 (VSMC) 经历代谢重编程,导致动脉样硬化斑块的异质性和不稳定性.
这种代谢转变推动了VSMC的表型变化,包括骨质性,巨类和泡细胞类状态.
VSMC代谢重编程与血管化,脂质积累和细胞外矩阵降解有关.

研究的目的:

在动脉样硬化 (AS) 发育期间审查VSMC表型.
阐明将代谢重编程与VSMC表型重塑联系起来的分子途径.
探索针对代谢调节者的治疗策略,以稳定斑块.

主要方法:

在AS中对VSMC表型的文献综述.
分析连接代谢重编程和VSMC命运的分子途径.
确定关键的代谢调节剂及其作用.
讨论代谢途径,表观遗传学和信号网络之间的相互作用.
探索治疗标和药剂的研究.

主要成果:

VSMC的代谢重编程驱动着不同的表型,并有助于AS的进展.
关键调节者,如葡萄糖转运体,pyruvate dehydrogenase kinase 4和脂肪酸合成酶,整合了代谢信号.
代谢途径与表观遗传和信号网络相互作用,以控制VSMC的增殖,亡,化和衰老.
有针对性的代谢干预措施显示出AS治疗的前景.

结论:

代谢重编程是动脉样硬化中VSMC表型可塑性的关键驱动因素.
了解这些代谢途径为稳定动脉样硬化斑块提供了新的治疗途径.
准代谢调节剂是管理AS进展的有希望的策略.

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