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

Biomed Pharmacother. 2020 Mar:123:109758. doi: 10.1016/j.biopha.2019.109758. Epub 2019 Dec 18.

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.

Keywords: Endothelin-1 signaling; Hyperhomocysteinemia; Phenotypic switching; Vascular smooth muscle cells.

Publication types

  • Review

MeSH terms

  • Animals
  • Atherosclerosis / metabolism
  • Cell Proliferation
  • Endothelin-1 / metabolism*
  • Humans
  • Hyperhomocysteinemia / metabolism*
  • Muscle, Smooth, Vascular / metabolism*
  • Myocytes, Smooth Muscle / metabolism*
  • Phenotype*
  • Phosphorylation
  • Signal Transduction

Substances

  • Endothelin-1