Vascular smooth muscle cells (VSMCs) are the major cell type in blood vessels. Unlike many other mature cell types in the adult body, VSMC do not terminally differentiate but retain a remarkable plasticity. Fully differentiated medial VSMCs of mature vessels maintain quiescence and express a range of genes and proteins important for contraction/dilation, which allows them to control systemic and local pressure through the regulation of vascular tone. In response to vascular injury or alterations in local environmental cues, differentiated/contractile VSMCs are capable of switching to a dedifferentiated phenotype characterized by increased proliferation, migration and extracellular matrix synthesis in concert with decreased expression of contractile markers. Imbalanced VSMC plasticity results in maladaptive phenotype alterations that ultimately lead to progression of a variety of VSMC-driven vascular diseases. The nature, extent and consequences of dysregulated VSMC phenotype alterations are diverse, reflecting the numerous environmental cues (e.g. biochemical factors, extracellular matrix components, physical) that prompt VSMC phenotype switching. In spite of decades of efforts to understand cues and processes that normally control VSMC differentiation and their disruption in VSMC-driven disease states, the crucial molecular mechanisms and signalling pathways that shape the VSMC phenotype programme have still not yet been precisely elucidated. In this article we introduce the physiological functions of vascular smooth muscle/VSMCs, outline VSMC-driven cardiovascular diseases and the concept of VSMC phenotype switching, and review molecular mechanisms that play crucial roles in the regulation of VSMC phenotypic plasticity.

血管平滑肌细胞（VSMC）是血管中的主要细胞类型。与成人体内许多其他成熟细胞类型不同，VSMC不会终末分化，但会保持出色的可塑性。成熟血管的完全分化的内侧VSMC保持静止并表达一系列对于收缩/扩张很重要的基因和蛋白质，这使它们可以通过调节血管张力来控制全身和局部压力。响应血管损伤或局部环境提示的变化，分化/收缩的VSMC能够转换为以分化增殖为特征的表型，其特征是增殖，迁移和细胞外基质合成增加，而收缩标志物的表达降低。VSMC可塑性不平衡会导致适应不良的表型改变，最终导致各种VSMC驱动的血管疾病的进展。VSMC表型改变失调的性质，程度和后果是多种多样的，反映了众多的环境提示（例如促使VSMC表型转换的生化因子，细胞外基质成分，物理）。尽管经过数十年的努力来理解通常可控制VSMC分化及其在VSMC驱动的疾病状态中被破坏的提示和过程，但仍无法精确阐明形成VSMC表型程序的关键分子机制和信号传导途径。在本文中，我们介绍了血管平滑肌/ VSMC的生理功能，概述了VSMC驱动的心血管疾病和VSMC表型转换的概念，并综述了在VSMC表型可塑性调节中起关键作用的分子机制。