Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, Chongqing Engineering Laboratory in Vascular Implants, College of Bioengineering, Chongqing University, , Chongqing 400044, People's Republic of China.
J R Soc Interface. 2013 Oct 23;11(90):20130852. doi: 10.1098/rsif.2013.0852. Print 2014 Jan 6.
Vascular smooth muscle cells (VSMCs) have critical functions in vascular diseases. Haemodynamic factors are important regulators of VSMC functions in vascular pathophysiology. VSMCs are physiologically active in the three-dimensional matrix and interact with the shear stress sensor of endothelial cells (ECs). The purpose of this review is to illustrate how haemodynamic factors regulate VSMC functions under two-dimensional conditions in vitro or three-dimensional co-culture conditions in vivo. Recent advances show that high shear stress induces VSMC apoptosis through endothelial-released nitric oxide and low shear stress upregulates VSMC proliferation and migration through platelet-derived growth factor released by ECs. This differential regulation emphasizes the need to construct more actual environments for future research on vascular diseases (such as atherosclerosis and hypertension) and cardiovascular tissue engineering.
血管平滑肌细胞（VSMCs）在血管疾病中具有关键功能。血流动力学因素是血管病理生理学中 VSMC 功能的重要调节剂。VSMCs 在三维基质中具有生理活性，并与内皮细胞（ECs）的切应力传感器相互作用。本综述的目的是说明血流动力学因素如何在体外二维条件或体内三维共培养条件下调节 VSMC 功能。最近的进展表明，高切应力通过内皮细胞释放的一氧化氮诱导 VSMC 凋亡，而低切应力通过 ECs 释放的血小板衍生生长因子上调 VSMC 的增殖和迁移。这种差异调节强调需要为未来血管疾病（如动脉粥样硬化和高血压）和心血管组织工程的研究构建更实际的环境。
