The Effect of Statins through Mast Cells in the Pathophysiology of Atherosclerosis: a Review

Curr Atheroscler Rep. 2020 May 26;22(5):19. doi: 10.1007/s11883-020-00837-9.

Abstract

Purpose of review: In this review, we discuss the evidence supporting the effects of statins on mast cells (MCs) in atherosclerosis and their molecular mechanism of action.

Recent findings: Statins or HMG-CoA reductase inhibitors are known for their lipid-lowering properties and are widely used in the prevention and treatment of cardiovascular diseases. There is growing evidence that statins have an inhibitory effect on MCs, which contributes to the pleiotropic effect of statins in various diseases. MCs are one of the crucial effectors of the immune system which play an essential role in the pathogenesis of multiple disorders. Recent studies have shown that MCs are involved in the development of atherosclerotic plaques. MCs secrete various inflammatory cytokines (IL-6, IL4, TNF-α, and IFNγ) and inflammatory mediators (histamine, tryptase, proteoglycans) after activation by various stimulants. This, in turn, will exacerbate atherosclerosis. Statins suppress the activation of MCs via IgE inhibition which leads to inhibition of inflammatory mediators and cytokines which are involved in the development and progression of atherosclerosis. In keeping with this evidence presented here, MCs can be considered as one of the therapeutic targets for statins in the treatment of atherosclerosis.

Keywords: Atherosclerosis; Inflammation; Mast cells; Statin.

Publication types

  • Review

MeSH terms

  • Animals
  • Atherosclerosis / drug therapy*
  • Atherosclerosis / physiopathology*
  • Cell Degranulation / drug effects
  • Cytokines / metabolism
  • Histamine Release / drug effects
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use*
  • Mast Cells / drug effects*
  • Mast Cells / immunology
  • Mast Cells / metabolism
  • Matrix Metalloproteinase Inhibitors / pharmacology
  • Matrix Metalloproteinase Inhibitors / therapeutic use
  • Phospholipase A2 Inhibitors / pharmacology
  • Phospholipase A2 Inhibitors / therapeutic use
  • Plaque, Atherosclerotic / physiopathology
  • Receptors, LDL / agonists
  • Toll-Like Receptors / antagonists & inhibitors
  • Toll-Like Receptors / metabolism

Substances

  • Cytokines
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • Matrix Metalloproteinase Inhibitors
  • Phospholipase A2 Inhibitors
  • Receptors, LDL
  • Toll-Like Receptors