| Literature DB >> 31864211 |
Yulong Chen1, Xingli Su2, Qiaohong Qin3, Yue Yu3, Min Jia4, Hongmei Zhang5, Huijin Li3, Leilei Pei6.
Abstract
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.Entities:
Keywords: Endothelin-1 signaling; Hyperhomocysteinemia; Phenotypic switching; Vascular smooth muscle cells
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Year: 2019 PMID: 31864211 DOI: 10.1016/j.biopha.2019.109758
Source DB: PubMed Journal: Biomed Pharmacother ISSN: 0753-3322 Impact factor: 6.529