TCF21: Flipping the Phenotypic Switch in SMC.
TCF21: Flipping the Phenotypic Switch in SMC.
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DOI：
10.1161/circresaha.120.316533
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发表时间：
2020-02
影响因子：
20.1
通讯作者：
Yi Xie;K. Martin
中科院分区：
文献类型：
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作者：
Yi Xie;K. Martin
血管平滑肌细胞(SMCs)的收缩特性允许动脉和小动脉调节血流和压力，以响应组织的紧急需求。这些构成血管中层的SMC还具有显著的表型可塑性，使它们能够适应更长时间的变化，从而允许伤口修复、生长和血管重塑。虽然许多细胞类型，包括骨骼和心肌细胞，经历了不可逆转的终末分化，但分化的SMC保留了去分化为不同表型的能力，这一过程被称为表型调制或转换。1研究最多的SMC表型转换发生在对血管损伤的反应中，成熟的SMC下调基因表达的收缩程序，重新进入细胞周期，成为迁移细胞，并分泌丰富的细胞外基质。这种合成的成纤维细胞样表型对于伤口修复是必不可少的，但也可能导致内膜增生和闭塞性病变。1
The contractile properties of vascular smooth muscle cells (SMCs) allow arteries and arterioles to regulate blood flow and pressure in response to acute demands of tissues. These SMCs that comprise the medial layer of vessels also possess a remarkable phenotypic plasticity that allows them to adapt to changes on a longer time scale, allowing for wound repair, growth, and vascular remodeling. While many cell types, including skeletal and cardiac myocytes, undergo irreversible terminal differentiation, differentiated SMC retain the ability to de-differentiate to distinct phenotypes, a process known as phenotypic modulation or switching. 1 The best-studied SMC phenotypic switch occurs in response to vascular injury, where mature SMC downregulate the contractile program of gene expression, re-enter the cell cycle, become migratory, and secrete copious extracellular matrix. This synthetic fibroblast-like phenotype is essential for wound repair but can also lead to intimal hyperplasia and occlusive lesions. 1