Mechanical programming of arterial smooth muscle cells in health and ageing.

Mechanical programming of arterial smooth muscle cells in health and ageing.
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DOI:
10.1007/s12551-021-00833-6
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发表时间:
2021-10
影响因子:
--
通讯作者:
Warren DT
Warren DT
中科院分区:
其他
文献类型:
--
作者:
Johnson RT;Solanki R;Warren DT

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动脉平滑肌细胞(ASMCs)是动脉壁内的主要细胞类型,可检测并响应外部机械力。这些力可以来自血流(即压力和拉伸)或来自支持细胞外基质(即刚度和形貌)。健康的动脉壁是弹性的,允许动脉改变形状以响应血压的变化,这一特性被称为动脉顺应性。随着年龄的增长,施加在ASMC上的机械力发生变化;血压和动脉壁硬度增加,导致动脉顺应性降低。这些机械环境的变化增强了ASMC的收缩力,并促进了ASMC表型的疾病相关变化。对于编程ASMCs的机械刺激,力必须影响细胞的承重装置,细胞骨架。由肌动蛋白丝、微管和中间丝的互连网络组成,每个细胞骨架组分具有不同的机械特性,使ASMC能够对机械环境中的变化做出反应,同时保持细胞的完整性。在这篇综述中,我们讨论了机械驱动的细胞骨架重组程序ASMC功能和表型转换。
Arterial smooth muscle cells (ASMCs), the predominant cell type within the arterial wall, detect and respond to external mechanical forces. These forces can be derived from blood flow (i.e. pressure and stretch) or from the supporting extracellular matrix (i.e. stiffness and topography). The healthy arterial wall is elastic, allowing the artery to change shape in response to changes in blood pressure, a property known as arterial compliance. As we age, the mechanical forces applied to ASMCs change; blood pressure and arterial wall rigidity increase and result in a reduction in arterial compliance. These changes in mechanical environment enhance ASMC contractility and promote disease-associated changes in ASMC phenotype. For mechanical stimuli to programme ASMCs, forces must influence the cell’s load-bearing apparatus, the cytoskeleton. Comprised of an interconnected network of actin filaments, microtubules and intermediate filaments, each cytoskeletal component has distinct mechanical properties that enable ASMCs to respond to changes within the mechanical environment whilst maintaining cell integrity. In this review, we discuss how mechanically driven cytoskeletal reorganisation programmes ASMC function and phenotypic switching.
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