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Pharmacological actions of statins: potential utility in COPD

R. P. Young, R. Hopkins, T. E. Eaton
European Respiratory Review 2009 18: 222-232; DOI: 10.1183/09059180.00005309
R. P. Young
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R. Hopkins
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T. E. Eaton
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  • FIGURE 1.
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    FIGURE 1.

    Proposed pathogenesis of chronic obstructive pulmonary disease. ROS: reactive oxygen species; LPS: lipopolysaccharide; PAH: polyaromatic hydrocarbons; BEC: bronchial epithelial cell; IL: interleukin; TNF: tumour necrosis factor; GM-CSF: granulocyte-monocyte colony-stimulating factor; TGF: transforming growth factor; PMN: polymorphic neutrophil; MPO: myeloperoxidase; MØ: macrophage; MMP: matrix metalloproteinase; NE: neutrophil elastatse; TIMP: tissue inhibitors of metalloproteinase; αAT: α1-antitrypsin; VEGF: vascular endothelial growth factor; END: endothelial cell; CRP: C-reactive protein. #: denotes the site of action of statins.

  • FIGURE 2.
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    FIGURE 2.

    Proposed pathogenesis of lung cancer. ECM: extracellular matrix; ROS: reactive oxygen species; LPS: lipopolysaccharide; PAH: polyaromatic hydrocarbons; HMG CoA: 3-hydroxy-3-methylglutaryl coenzyme A; GTPase; guanosine triphosphatase; SHH: sonic hedgehog homologue; NADPH: reduced nicotinamide adenine dinucleotide phosphate; EGFR: epidermal growth factor receptor; TGF: transforming growth factor; NF-κB: nuclear factor-κB; AP-1: activator protein-1; MMP: matrix metalloproteinase; MPO: myeloperoxidase; PMN: polymorphic neutrophil; FGF: fibroblast growth factor. #: denotes the site of action of statins.

  • FIGURE 3.
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    FIGURE 3.

    Morbidity and mortality benefits with statin use in observational studies on a logarithmic scale. CVS: cardiovascular; COPD: chronic obstructive pulmonary disease. Data are presented as odds ratio (95% confidence interval), except hospital cohort which is presented as relative risk (95% confidence interval) and following COPD exacerbation which is presented as hazard ratio (95% confidence interval).

Tables

  • Figures
  • Table. 1—

    Summary of statin mediated pharmacological effects on pulmonary inflammation and remodeling

    COPD pathwayStudy typeStatin effect on pathogenic pathways[Ref.]
    Cytokine productionMM, HM in vitro (liver cell line), HM in vivo (mononuclear cells)Reduce IL-6 induced CRP production by hepatocytes[52, 67, 68]
    HM in vitro (VSM cells and PBE cells)Reduce IL-8 production by VSM cells[69, 70]
    MMInhibition of neutrophil accumulation and IL-8 and TNF-α concentration in BALF in rats[71]
    HM in vivo (serum), MMReduce production of IL-β1 and TNF-α[52, 72]
    MMReduced expression of IFN-γ TNF-α and MMP12 in whole lung[73]
    Matrix remodellingMMReduced lung parenchymal destruction and MMP 9 activity in smoke exposed rat lung[74, 75]
    HM ex vivo (bronchial epithelial cells)Reduce release of MMP2 and MMP9 from bronchial epithelial cells from lung transplant patients[70]
    Neutrophil/macrophage influxHM ex vivo (bronchial epithelial cells), HM in vivo (PMN)Reduce neutrophil influx in lung transplant recipients by inhibiting release of IL-8 and GM-CSF from bronchial epithelial cells[70, 76, 77]
    HM in vitro (PMN), HM in vivo (serum)Reduce neutrophil endothelial adhesion and transendothelial migration[76, 78–80]
    MMReduce neutrophil influx and inhibit the development of elastase induced pulmonary emphysema in mice[74, 75]
    MM, HM ex vivo (human monocytes)Reduce CRP-induced monocyte migration by inhibition of ICAM-1 in human monocytes[81]
    MM, HM in vitro (endothelial cells), HM in vivo (BALF)Reduced concentration of neutrophils and lymphocytes in BALF[74, 75]
    MM, HM in vitroReduce chemokine and adhesion molecule expression to reduce migration of inflammatory cells into the airways[74, 81, 82]
    Epithelial/endothelial integrityMMPromotes alveolar cell regeneration and restores endothelial cell function[75]
    MMReduce LPS-induced IL-6 gene expression leading to reduced lung vascular leak and pulmonary inflammation in mice lung[83]
    HM in vitro (endothelial and smooth muscle cells)Inhibition of VEGF in smooth muscle cells and endothelial cells[84]
    ApoptosisHM in vitro (macrophages and PMN)Enhances clearance of apoptotic cells in alveolar macrophages from patients with COPD[85]
    HM in vitro (endothelial cells), HM in vitro (endothelial and smooth muscle cells)Increase apoptosis in human vascular endothelial cells[84, 86]
    Oxidant responseHM in vivo (PMN)Reduce IL-8 release from neutrophils and neutrophil derived reactive oxidant species[77]
    HM in vivo (serum), MMStrong anti-oxidant properties[87, 88]
    Mucus productionMMReduced LPS-induced goblet cell hyperplasia in bronchial epithelium and Muc5A induced mucus hypersecretion[71]
    CRP levelHM in vitro (liver cell)Reduce CRP levels at the transcriptional level thorough Rac-1 mediated inhibition of STAT3 phosphorylation[67]
    • COPD: chronic obstructive pulmonary disease; CRP: C-reactive protein; MM: murine model; HM: human model; VSM: vascular smooth muscle; PBE: primary bronchial epithelial; PMN: polymorphic neutrophil; BALF: bronchoalveolar lavage fluid; IL: interleukin; TNF: tumour necrosis factor; IFN: interferon; MMP: matrix metalloproteinase; GM-CSF: granulocyte-monocyte colony-stimulating factor; ICAM: intracellular adhesion molecule; LPS: lipopolysaccharide; VEGF: vascular endothelial growth factor.

  • Table. 2—

    Mortality benefit of statin use in the general population diagnosed with community acquired pneumonia

    CohortSubject nRisk reduction[Ref.]
    Retrospective cohort study in teaching hospital7870.36 (0.14–0.92)64% reduction in 30-day mortality[102]
    Population based prospective cohort study34150.78 (0.57–1.07)22% reduction in mortality or admission to an ICU[103]
    Population based retrospective nested case–control60890.47 (0.25–0.88)53% reduction in fatal pneumonia[104]
    Prospective hospital based observational study10070.46 (0.25–0.85)54% reduction in 30-day mortality[105]
    Population based cohort study299000.69 (0.58–0.82)31% reduction in 30-day mortality[106]
    0.75 (0.65–0.86)25% reduction in 90-day mortality
    Retrospective national cohort study86520.54 (0.42–0.70)46% reduction in 30-day mortality[107]
    Population based case–control study22350.81 (0.46–1.42)19% reduction in risk of pneumonia (after excluding those with CAD)[108]
    Population based cohort study36810.33 (0.19–0.58)67% reduction in 30-day mortality[109]
    0.45 (0.32–0.62)55% reduction in long-term mortality
    • Data are presented as odds ratio (95% confidence interval). Data for population based case–control study and cohort study are presented as hazard ration (95% confidence interval). ICU: intensive care unit; CAD: coronary artery disease.

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Pharmacological actions of statins: potential utility in COPD
R. P. Young, R. Hopkins, T. E. Eaton
European Respiratory Review Dec 2009, 18 (114) 222-232; DOI: 10.1183/09059180.00005309

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Pharmacological actions of statins: potential utility in COPD
R. P. Young, R. Hopkins, T. E. Eaton
European Respiratory Review Dec 2009, 18 (114) 222-232; DOI: 10.1183/09059180.00005309
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  • Article
    • Abstract
    • PATHOPHYSIOLOGY OF COPD
    • EPIDEMIOLOGY OF COPD
    • CURRENT TREATMENT IN COPD
    • COPD AND SYSTEMIC INFLAMMATION
    • STATIN EFFECTS ON CLINICAL OUTCOMES IN COPD: AN OVERVIEW
    • STATINS EFFECTS ON SYSTEMIC INFLAMMATION IN COPD
    • STATIN EFFECTS ON PULMONARY INFLAMMATION IN COPD
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  • Methods to assess COPD medications adherence in healthcare databases
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