Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 123, Issue -, Pages -Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2019.109758
Keywords
Hyperhomocysteinemia; Phenotypic switching; Vascular smooth muscle cells; Endothelin-1 signaling
Funding
- Science and Technology Innovation Base-Open and Sharing Platform of Science and Technology Resources Project of Shaanxi Province [2019PT-26]
- Revitalizing Talent Fund Project [2018XNRC04]
- Cultivation Fund of the National Natural Science Foundation of China [2018GJFY07]
- Xi'an Medical University [2016PT27, 2017PT01, 2017PT39]
- Key Scientific Research Plan Project of Education Department of Shaanxi Province [18JS103]
- National Natural Science Foundation of China [81602928]
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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.
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