title: Is the aging process accelerated in chronic obstructive pulmonary disease?
abstract: OBJECTIVE
  Recent research suggests that chronic obstructive pulmonary disease (COPD) may be a disease of accelerated aging. The senescence hypothesis of COPD pathogenesis is supported by in-vitro, in-vivo and clinical studies. The purpose of this review is to provide a comprehensive overview of the senescence hypothesis of COPD and summarize methods that are used to assess cellular aging.
  
  
  RESULTS
  Accelerated aging due to exposure to cigarette smoke is hypothesized to induce rapid progression of COPD. Recent studies have shown that COPD patients have enhanced expression of senescence-associated proteins in the lung and in the peripheral circulation compared to healthy controls. Murine models of accelerated aging demonstrate spontaneous emphysematous changes in the lungs, while lungs of COPD patients demonstrate enhanced markers of senescence in fibroblasts and alveolar cells. More recently, studies of telomeres, which shorten with cellular aging, have shown that COPD patients may experience accelerated telomere attrition compared with healthy controls. However, studies to date have been relatively small and have produced heterogeneous results.
  
  
  CONCLUSIONS
  The evidence for the role of accelerated aging in COPD progression is growing and senescence is one possible molecular pathway by which COPD occurs.
authors.affiliation: Department of Medicine and the Providence Heart and Lung Institute at St. Paul’s Hospital, The University of British Columbia James Hogg Research Centre, Vancouver, British Columbia, Canada.
authors.forename: Jee
authors.initials: J
authors.lastname: Lee
authors.forename: Andrew
authors.initials: A
authors.lastname: Sandford
authors.forename: Paul
authors.initials: P
authors.lastname: Man
authors.forename: Don D
authors.initials: DD
authors.lastname: Sin
mesh_terms: D000375:Aging / Q000502:physiology*; D015415:Biomarkers / Q000737:chemistry; D015139:Blotting, Southern; D016922:Cellular Senescence / Q000502:physiology*; D018450:Disease Progression; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D007962:Leukocytes / Q000502:physiology; D018384:Oxidative Stress / Q000502:physiology; D016133:Polymerase Chain Reaction; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology / Q000503:physiopathology*; D016615:Telomere / Q000502:physiology / Q000648:ultrastructure
chemical_list: D015415:Biomarkers