13. COPD as a Disease of Premature Aging

  1. Mauricio Rojas2,3,4,
  2. Silke Meiners5,6 and
  3. Claude Jourdan Le Saux7
  1. Laurent Boyer,
  2. Jorge Boczkowski and
  3. Serge Adnot

Published Online: 28 MAR 2014

DOI: 10.1002/9781118396292.ch13

Molecular Aspects of Aging: Understanding Lung Aging

Molecular Aspects of Aging: Understanding Lung Aging

How to Cite

Boyer, L., Boczkowski, J. and Adnot, S. (2014) COPD as a Disease of Premature Aging, in Molecular Aspects of Aging: Understanding Lung Aging (eds M. Rojas, S. Meiners and C. J. Le Saux), John Wiley & Sons, Inc, Hoboken, NJ. doi: 10.1002/9781118396292.ch13

Editor Information

  1. 2

    Dorothy P. and Richard P. Simmons Center for Interstitial Lung Diseases

  2. 3

    Division of Pulmonary, Allergy and Critical Care Medicine

  3. 4

    McGowan Institute for Regenerative Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA

  4. 5

    Comprehensive Pneumology Center (CPC), University Hospital, Ludwig-Maximilians-University, Helmholtz Zentrum München

  5. 6

    Member of the German Center for Lung Research (DZL), Munich, Germany

  6. 7

    University of Texas Health Science Center, Division of Cardiology and Pulmonary and Critical Care, San Antonio, Texas, USA

Author Information

  1. INSERM U955 and Département de Physiologie-Explorations Fonctionnelles, Hôpital Henri Mondor, Université Paris Est, Paris, France

Publication History

  1. Published Online: 28 MAR 2014
  2. Published Print: 20 MAR 2014

ISBN Information

Print ISBN: 9781118396247

Online ISBN: 9781118396292

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Keywords:

  • chronic obstructive pulmonary disease (COPD);
  • lung dysfunction;
  • lung-cell senescence;
  • premature aging;
  • senescent cells

Summary

Chronic obstructive pulmonary disease (COPD) is an age-related disease for which new data indicate associations with telomere shortening and exaggerated cell senescence. A unifying concept is that lung alterations contribute to drive the process of systemic senescence and premature aging in COPD, even in patients with only moderate degrees of lung dysfunction. Thus, elucidating the mechanisms that underlie premature aging in COPD would probably produce major clinical benefits. This chapter discusses two concepts relevant to current research on these mechanisms: (i) senescent cells contribute to pathogenesis of COPD, and (ii) lung alterations contribute to drive the process of systemic senescence and premature aging and the development of comorbidities in COPD.