New insights into phenotypic switching of VSMCs induced by hyperhomocysteinemia: Role of endothelin-1 signaling

Biomedicine & Pharmacotherapy

卷:123

Qiaohong Qin¹  Min Jia²  Xingli Su³  Yulong Chen⁴  Hongmei Zhang⁴  Leilei Pei⁴  Huijin Li⁴  Yue Yu⁵ 

[1]Corresponding author at: Institute of Basic and Translational Medicine, Shaanxi Key Laboratory of Ischemic Cardiovascular Disease, Shaanxi Key Laboratory of Brain Disorders, Xi'an Medical University, Xi'an, Shaanxi, 710021, China.

[2]|Corresponding author.

[3]|School of Basic and Medical Sciences, Xi’an Medical University, Xi’an, Shaanxi, 710021, China

[4]|Institute of Basic and Translational Medicine, Shaanxi Key Laboratory of Ischemic Cardiovascular Disease, Shaanxi Key Laboratory of Brain Disorders, Xi’an Medical University, Xi’an, Shaanxi, 710021, China

[5]|School of Basic and Medical Sciences, Xi’an Medical University, Xi’an, Shaanxi, 710021, China

关键词: Hyperhomocysteinemia;    Phenotypic switching;    Vascular smooth muscle cells;    Endothelin-1 signaling;   

DOI  :  

来源: DOAJ

【 摘 要 】

Phenotypic switching of vascular smooth muscle cells (VSMCs) plays a key role in atherosclerosis. Hyperhomocysteinemia (HHcy) is an independent risk factor for atherosclerosis. HHcy induces phenotypic switching of VSMCs, but the mechanism is unclear. Endothelin-1 (ET-1) promotes proliferation and migration of VSMCs by inducing phenotypic switching during atherosclerosis. This review examined recent findings on the relationship between HHcy or the ET-1 system (including ET-1 and its receptors) and phenotypic switching of VSMCs as well as the molecular mechanism of HHcy-regulated ET-1 signaling. In particular, we focused on the potential mechanisms and pharmacological targets of phenotypic switching of VSMCs regulated by HHcy through ET-1 signaling.

【 授权许可】

Unknown