Aguilar Victor M, Paul Amit, Lazarko Dana, Levitan Irena
Department of Medicine, Division of Pulmonary and Critical Care, College of Medicine, University of Illinois at Chicago, Chicago, IL, United States.
Richard and Loan Hill Department of Biomedical Engineering, University of Illinois at Chicago, Chicago, IL, United States.
Front Physiol. 2023 Jan 11;13:1081119. doi: 10.3389/fphys.2022.1081119. eCollection 2022.
Endothelial cells, the inner lining of the blood vessels, are well-known to play a critical role in vascular function, while endothelial dysfunction due to different cardiovascular risk factors or accumulation of disruptive mechanisms that arise with aging lead to cardiovascular disease. In this review, we focus on endothelial stiffness, a fundamental biomechanical property that reflects cell resistance to deformation. In the first part of the review, we describe the mechanisms that determine endothelial stiffness, including RhoA-dependent contractile response, actin architecture and crosslinking, as well as the contributions of the intermediate filaments, vimentin and lamin. Then, we review the factors that induce endothelial stiffening, with the emphasis on mechanical signals, such as fluid shear stress, stretch and stiffness of the extracellular matrix, which are well-known to control endothelial biomechanics. We also describe in detail the contribution of lipid factors, particularly oxidized lipids, that were also shown to be crucial in regulation of endothelial stiffness. Furthermore, we discuss the relative contributions of these two mechanisms of endothelial stiffening in vasculature in cardiovascular disease and aging. Finally, we present the current state of knowledge about the role of endothelial stiffening in the disruption of endothelial cell-cell junctions that are responsible for the maintenance of the endothelial barrier.
内皮细胞作为血管的内层,在血管功能中发挥关键作用,这是众所周知的。而由于不同的心血管危险因素或随着衰老出现的破坏机制的积累所导致的内皮功能障碍会引发心血管疾病。在本综述中,我们聚焦于内皮硬度,这是一种反映细胞对变形抵抗力的基本生物力学特性。在综述的第一部分,我们描述了决定内皮硬度的机制,包括 RhoA 依赖性收缩反应、肌动蛋白结构和交联,以及中间丝、波形蛋白和层粘连蛋白的作用。然后,我们回顾了诱导内皮变硬的因素,重点是机械信号,如流体剪切应力、拉伸和细胞外基质的硬度,这些信号在控制内皮生物力学方面是众所周知的。我们还详细描述了脂质因子,特别是氧化脂质的作用,它们在调节内皮硬度方面也被证明至关重要。此外,我们讨论了这两种内皮变硬机制在心血管疾病和衰老过程中血管系统中的相对作用。最后,我们介绍了关于内皮变硬在破坏负责维持内皮屏障的内皮细胞间连接中作用的当前知识状态。