Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, 415 Lane Road, PO Box 801394, Room 1322 Medical Research Building 5, Charlottesville, VA 22908, USA.
Cardiovasc Res. 2012 Jul 15;95(2):156-64. doi: 10.1093/cvr/cvs115. Epub 2012 Mar 8.
Smooth muscle cells (SMCs) possess remarkable phenotypic plasticity that allows rapid adaptation to fluctuating environmental cues, including during development and progression of vascular diseases such as atherosclerosis. Although much is known regarding factors and mechanisms that control SMC phenotypic plasticity in cultured cells, our knowledge of the mechanisms controlling SMC phenotypic switching in vivo is far from complete. Indeed, the lack of definitive SMC lineage-tracing studies in the context of atherosclerosis, and difficulties in identifying phenotypically modulated SMCs within lesions that have down-regulated typical SMC marker genes, and/or activated expression of markers of alternative cell types including macrophages, raise major questions regarding the contributions of SMCs at all stages of atherogenesis. The goal of this review is to rigorously evaluate the current state of our knowledge regarding possible phenotypes exhibited by SMCs within atherosclerotic lesions and the factors and mechanisms that may control these phenotypic transitions.
平滑肌细胞（SMCs）具有显著的表型可塑性，使其能够快速适应不断变化的环境线索，包括在血管疾病如动脉粥样硬化的发展和进展过程中。尽管人们已经了解了许多控制培养细胞中 SMC 表型可塑性的因素和机制，但我们对控制体内 SMC 表型转换的机制的了解还远远不够。事实上，在动脉粥样硬化背景下缺乏明确的 SMC 谱系追踪研究，以及在下调典型 SMC 标记基因和/或激活包括巨噬细胞在内的替代细胞类型标记物的表达的病变中识别表型调节的 SMC 存在困难，这使得人们对 SMC 在动脉粥样形成的所有阶段的贡献提出了重大问题。本综述的目的是严格评估我们目前对动脉粥样硬化病变中 SMC 可能表现出的表型以及可能控制这些表型转变的因素和机制的了解。
