Acid fibroblast growth factor facilitates the progression of atherosclerotic plaques regardless of alterations in serum lipid expression levels in HFD‑fed ApoE‑/‑ mice

Mol Med Rep. 2018 Jul;18(1):1025-1030. doi: 10.3892/mmr.2018.9060. Epub 2018 May 23.

Abstract

Atherosclerosis is recognized at present as a chronic metabolic disease of the arteries that leads to multifocal plaque development. Previous studies have reported that acid fibroblast growth factor (aFGF) is a critical therapeutic regulator in numerous chronic metabolic disorders. However, there is currently no direct evidence indicating whether aFGF serves a therapeutic role in atherosclerosis. In the present study, the role of aFGF in atherosclerotic lesion development was investigated by examining high‑fat diet (HFD)‑fed apolipoprotein E (ApoE)‑/‑ mice and parenteral administration of aFGF. Increased expression of aFGF and peroxisome proliferator‑activated receptor α (PPARα) was observed during atherosclerotic lesion development. The parenteral delivery of aFGF facilitated the progression of atherosclerosis without altering serum lipid expression levels in HFD‑fed ApoE‑/‑ mice. Furthermore, it was demonstrated that aFGF increased the expression of PPARα and inflammatory cytokines. The present results provided evidence that aFGF accelerates the progression of atherosclerosis and suggested that aFGF may be a potential therapeutic target for the prevention of atherosclerosis development.

MeSH terms

  • Animals
  • Apolipoproteins E / deficiency*
  • Atherosclerosis* / chemically induced
  • Atherosclerosis* / genetics
  • Atherosclerosis* / metabolism
  • Atherosclerosis* / pathology
  • Dietary Fats / adverse effects*
  • Dietary Fats / pharmacology
  • Fibroblast Growth Factor 1* / genetics
  • Fibroblast Growth Factor 1* / metabolism
  • Mice
  • Mice, Knockout
  • PPAR alpha / genetics
  • PPAR alpha / metabolism
  • Plaque, Atherosclerotic* / chemically induced
  • Plaque, Atherosclerotic* / genetics
  • Plaque, Atherosclerotic* / metabolism
  • Plaque, Atherosclerotic* / pathology

Substances

  • Apolipoproteins E
  • Dietary Fats
  • PPAR alpha
  • Fibroblast Growth Factor 1