9
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Abnormal lung aging in chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis.

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Aging is a natural process characterized by progressive functional impairment and reduced capacity to respond appropriately to environmental stimuli and injury. The incidence of two common chronic respiratory diseases (chronic obstructive pulmonary disease [COPD] and idiopathic pulmonary fibrosis [IPF]) increases with advanced age. It is plausible, therefore, that abnormal regulation of the mechanisms of normal aging may contribute to the pathobiology of both COPD and IPF. This review discusses the available evidence supporting a number of aging mechanisms, including oxidative stress, telomere length regulation, cellular and immunosenescence, as well as changes in a number of antiaging molecules and the extracellular matrix, which are abnormal in COPD and/or IPF. A better understanding of these abnormalities may help in the design of novel and better therapeutic interventions for these patients.

          Related collections

          Author and article information

          Journal
          Am J Respir Crit Care Med
          American journal of respiratory and critical care medicine
          American Thoracic Society
          1535-4970
          1073-449X
          Aug 15 2012
          : 186
          : 4
          Affiliations
          [1 ] Fundación Investigación Sanitaria Illes Balears, Centro de Investigación Biomédica en Red Enfermedades Respiratorias (CIBERES), Palma de Mallorca, and Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
          Article
          rccm.201202-0282PP
          10.1164/rccm.201202-0282PP
          22582162
          7a87672b-e823-4176-8aaa-a91393be124f
          History

          Comments

          Comment on this article