Jee Lee1, Andrew Sandford, Paul Man, Don D Sin. 1. 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.
Abstract
PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: The evidence for the role of accelerated aging in COPD progression is growing and senescence is one possible molecular pathway by which COPD occurs.
PURPOSE OF REVIEW: 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. RECENT FINDINGS: Accelerated aging due to exposure to cigarette smoke is hypothesized to induce rapid progression of COPD. Recent studies have shown that COPDpatients 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 COPDpatients demonstrate enhanced markers of senescence in fibroblasts and alveolar cells. More recently, studies of telomeres, which shorten with cellular aging, have shown that COPDpatients may experience accelerated telomere attrition compared with healthy controls. However, studies to date have been relatively small and have produced heterogeneous results. SUMMARY: 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: Joanna Smolonska; Gerard H Koppelman; Cisca Wijmenga; Judith M Vonk; Pieter Zanen; Marcel Bruinenberg; Ivan Curjuric; Medea Imboden; Gian-Andri Thun; Lude Franke; Nicole M Probst-Hensch; Peter Nürnberg; Roland A Riemersma; Constant P van Schayck; Daan W Loth; Guy G Brusselle; Bruno H Stricker; Albert Hofman; André G Uitterlinden; Lies Lahousse; Stephanie J London; Laura R Loehr; Ani Manichaikul; R Graham Barr; Kathleen M Donohue; Stephen S Rich; Peter Pare; Yohan Bossé; Ke Hao; Maarten van den Berge; Harry J M Groen; Jan-Willem J Lammers; Willem Mali; H Marike Boezen; Dirkje S Postma Journal: Eur Respir J Date: 2014-07-03 Impact factor: 16.671
Authors: Jee Lee; Andrew J Sandford; John E Connett; Jin Yan; Tammy Mui; Yuexin Li; Denise Daley; Nicholas R Anthonisen; Angela Brooks-Wilson; S F Paul Man; Don D Sin Journal: PLoS One Date: 2012-04-25 Impact factor: 3.240