CVD中VSMC炎症的表观遗传猝灭:H3K9me2在控制中。

E. Lutgens
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引用次数: 2

摘要

根据动脉粥样硬化斑块发展的旧教条,血管平滑肌细胞(VSMCs)是动脉粥样硬化斑块生长纤维帽的基质产生引擎,并负责维持斑块的稳定性斑块VSMCs最初是介质中的收缩VSMCs,在损伤时,它们被招募到内膜,并经历表型转化为增殖合成细胞,产生并沉积细胞外基质
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Epigenetic Quenching of VSMC Inflammation in CVD: H3K9me2 in Control.
According to the old dogma of atherosclerotic plaque development, vascular smooth muscle cells (VSMCs) are the matrix-producing engines of the atherosclerotic plaque that grow the fibrous cap and are a responsible for maintaining plaque stability.1 Plaque VSMCs start of as contractile VSMCs in the media, where they, on injury, are recruited to the intima and undergo phenotypic conversion toward proliferative synthetic cells that produce and deposit extracellular matrix.1
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