摘要
主动脉疾病(aortic disease,AD)指由于主动脉壁病变所致的一类疾病,往往高度致命。目前非遗传性AD的发病机制尚未完全阐明。血管平滑肌细胞(vascular smooth muscle cells,VSMC)是主动脉壁中层的主要细胞成分,通常认为其存在收缩型与合成型两种表型,且可相互转化。VSMC由收缩型向合成型的过度转化在AD的发生发展过程起重要作用。尽管关于VSMC表型转化研究较多,但众多调控机制如何协调运作以及相互之间的关系仍然有待阐明。本文就目前已知的VSMC表型转化调控机制作一综述。
Aortic disease(AD) consists of a series of life-threatening diseases caused by aortic wall lesions. Up to now little has been known about the etiology of non-hereditary AD. Vascular smooth muscle cells(VSMC) are the major components of the medial aortic wall and can toggle between a contractile phenotype and a synthetic phenotype. The excessive transformation of VSMC from contractile state to synthetic state plays an important role in the development and progression of AD. Although there are many researches on the regulation of VSMS phenotype switch, how these regulatory pathways operate harmoniously and the what relationship between them remain to be elucidated. Here in this paper we reviewed the existing regulatory mechanisms of VSMC phenotype switch.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2016年第8期992-995,共4页
Academic Journal of Second Military Medical University