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颅内动脉瘤中的血管平滑肌细胞。

Vascular smooth muscle cells in intracranial aneurysms.

作者信息

Wang Zhenye, Ma Jia, Yue Hongyan, Zhang Zhewei, Fang Fei, Wang Guixue, Liu Xiaoheng, Shen Yang

机构信息

Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.

Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China; Jinfeng Laboratory, Chongqing 401329, China.

出版信息

Microvasc Res. 2023 Sep;149:104554. doi: 10.1016/j.mvr.2023.104554. Epub 2023 May 24.

DOI:10.1016/j.mvr.2023.104554
PMID:37236346
Abstract

Intracranial aneurysm (IA) is a severe cerebrovascular disease characterized by abnormal bulging of cerebral vessels that may rupture and cause a stroke. The expansion of the aneurysm accompanies by the remodeling of vascular matrix. It is well-known that vascular remodeling is a process of synthesis and degradation of extracellular matrix (ECM), which is highly dependent on the phenotype of vascular smooth muscle cells (VSMCs). The phenotypic switching of VSMC is considered to be bidirectional, including the physiological contractile phenotype and alternative synthetic phenotype in response to injury. There is increasing evidence indicating that VSMCs have the ability to switch to various phenotypes, including pro-inflammatory, macrophagic, osteogenic, foamy and mesenchymal phenotypes. Although the mechanisms of VSMC phenotype switching are still being explored, it is becoming clear that phenotype switching of VSMCs plays an essential role in IA formation, progression, and rupture. This review summarized the various phenotypes and functions of VSMCs associated with IA pathology. The possible influencing factors and potential molecular mechanisms of the VSMC phenotype switching were further discussed. Understanding how phenotype switching of VSMC contributed to the pathogenesis of unruptured IAs can bring new preventative and therapeutic strategies for IA.

摘要

颅内动脉瘤(IA)是一种严重的脑血管疾病,其特征是脑血管异常膨出,可能破裂并导致中风。动脉瘤的扩张伴随着血管基质的重塑。众所周知,血管重塑是细胞外基质(ECM)合成与降解的过程,高度依赖于血管平滑肌细胞(VSMC)的表型。VSMC的表型转换被认为是双向的,包括生理收缩表型和损伤后出现的替代合成表型。越来越多的证据表明,VSMC能够转换为多种表型,包括促炎、巨噬细胞、成骨、泡沫细胞和间充质表型。尽管VSMC表型转换的机制仍在探索中,但越来越清楚的是,VSMC的表型转换在IA的形成、进展和破裂中起着至关重要的作用。本综述总结了与IA病理相关的VSMC的各种表型和功能。进一步讨论了VSMC表型转换的可能影响因素和潜在分子机制。了解VSMC表型转换如何促成未破裂IA的发病机制可为IA带来新的预防和治疗策略。

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