Shihata Waled A, Michell Danielle L, Andrews Karen L, Chin-Dusting Jaye P F
Cardiovascular Disease Program and Department of Pharmacology, Biomedical Discovery Institute, Monash UniversityClayton, VIC, Australia; Vascular Pharmacology, Baker IDI Heart and Diabetes InstituteMelbourne, VIC, Australia.
Vascular Pharmacology, Baker IDI Heart and Diabetes Institute Melbourne, VIC, Australia.
Front Physiol. 2016 Dec 20;7:628. doi: 10.3389/fphys.2016.00628. eCollection 2016.
Vascular inflammation and disease progression, such as atherosclerosis, are in part a consequence of haemodynamic forces generated by changes in blood flow. The haemodynamic forces, such as shear stress or stretch, interact with vascular endothelial cells, which transduce the mechanical stimuli into biochemical signals via mechanosensors, which can induce an upregulation in pathways involved in inflammatory signaling. However, it is unclear how these mechanosensors respond to shear stress and most significantly what cellular mechanisms are involved in sensing the haemodynamic stimuli. This review explores the transition from shear forces, stretch and pressure to endothelial inflammation and the process of mechanotransduction, specifically highlighting evidence to suggest that caveolae play as a role as mechanosensors.
血管炎症和疾病进展，如动脉粥样硬化，部分是血流变化所产生的血流动力学力的结果。血流动力学力，如剪切应力或拉伸力，与血管内皮细胞相互作用，血管内皮细胞通过机械传感器将机械刺激转化为生化信号，这可诱导炎症信号传导相关通路的上调。然而，尚不清楚这些机械传感器如何响应剪切应力，最重要的是，感知血流动力学刺激涉及哪些细胞机制。本综述探讨了从剪切力、拉伸和压力到内皮炎症的转变以及机械转导过程，特别强调了表明小窝作为机械传感器发挥作用的证据。
