Fibroblast growth factor 21 potentially inhibits microRNA-33 expression to affect macrophage actions

Lipids Health Dis. 2016 Dec 1;15(1):208. doi: 10.1186/s12944-016-0381-6.

Abstract

Atherosclerosis is a chronic inflammatory disease with complex pathological processes. MicroRNA-33 (miR-33), a novel non-coding RNA that coexpresses with sterol regulatory element-binding proteins (SREBPs), affects macrophage actions to prevent atherosclerosis. Fibroblast growth factor 21 (FGF21) is an important regulator of lipid metabolism, especially for macrophage-related cholesterol export, but the mechanism is not fully studied. Interestingly, FGF21 has been evidenced to prevent atherosclerosis via inhibiting SREBP-2 expression. Therefore, we speculate that FGF21 may be a potential regulator for miR-33 with an aim of insight into novel anti-atherosclerotic mechanisms and research fields.

Keywords: Atherosclerosis; Fibroblast growth factor 21; MicroRNA-33.

Publication types

  • Editorial
  • Review

MeSH terms

  • Animals
  • Atherosclerosis / genetics
  • Atherosclerosis / metabolism
  • Atherosclerosis / pathology*
  • Fibroblast Growth Factors / genetics
  • Fibroblast Growth Factors / metabolism*
  • Gene Expression Regulation
  • Humans
  • Macrophages / pathology
  • Macrophages / physiology*
  • Mice
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Sterol Regulatory Element Binding Protein 2 / genetics
  • Sterol Regulatory Element Binding Protein 2 / metabolism

Substances

  • MIRN33a microRNA, human
  • MicroRNAs
  • Mirn33 microRNA, mouse
  • SREBF2 protein, human
  • Sterol Regulatory Element Binding Protein 2
  • fibroblast growth factor 21
  • Fibroblast Growth Factors