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Potential therapeutic role for statins in respiratory disease
  1. E Hothersall1,
  2. C McSharry2,
  3. N C Thomson1
  1. 1Department of Respiratory Medicine, Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow, UK
  2. 2Department of Immunology, Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow, UK
  1. Correspondence to:
    Professor N C Thomson
    Department of Respiratory Medicine, Division of Immunology, Infection and Inflammation, Western Infirmary and University of Glasgow, Glasgow G11 6NT, UK; n.c.thomson{at}clinmed.gla.ac.uk

Abstract

Statins reduce cholesterol levels by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and have an established role in the treatment of atherosclerotic disease. Recent research has identified anti-inflammatory properties of statins. Statins appear to reduce the stability of lipid raft formation with subsequent effects on immune activation and regulation, and also prevent the prenylation of signalling molecules with subsequent downregulation of gene expression. Both these effects result in reduced cytokine, chemokine, and adhesion molecule expression, with effects on cell apoptosis or proliferation. This review considers the evidence for the anti-inflammatory properties of statins in the lung, and how these effects are being applied to research into the role of statins as a novel treatment of respiratory diseases.

  • CCL2, chemoattractant chemokine ligand 2
  • COPD, chronic obstructive pulmonary disease
  • CRP, C-reactive protein
  • CTGF, connective tissue growth factor
  • HMG-CoA, 3-hydroxy-3-methylglutaryl coenzyme A
  • IFN-γ, interferon γ
  • ICAM-1, intercellular adhesion molecule 1
  • IL, interleukin
  • IPF, idiopathic pulmonary fibrosis
  • LFA-1, lymphocyte function associated antigen 1
  • LPS, lipopolysaccharide
  • MHC-II, major histocompatibility complex class II
  • MMP, metalloprotease
  • NF-κB, nuclear factor κB
  • NK, natural killer
  • TGF-β, transforming growth factor β
  • TNF-α, tumour necrosis factor α
  • asthma
  • chronic obstructive pulmonary disease
  • statins
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Footnotes

  • This study was funded by Asthma UK.

  • Competing interests: none declared

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