Influence of age on wound healing and fibrosis

Authors

  • Maria G Kapetanaki,

    Corresponding author
    1. Dorothy P and Richard P Simmons Center for Interstitial Lung Disease, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    2. Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    • Correspondence to: M Rojas, UPMC Montefiore Hospital, NW628, 3459 Fifth Avenue, Pittsburgh, PA 15213, USA. e-mail: rojasm@upmc.edu

    Search for more papers by this author
  • Ana L Mora,

    1. Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    2. Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    Search for more papers by this author
  • Mauricio Rojas

    Corresponding author
    1. Dorothy P and Richard P Simmons Center for Interstitial Lung Disease, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    2. Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    3. McGowan Institute for Regenerative Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    • Correspondence to: M Rojas, UPMC Montefiore Hospital, NW628, 3459 Fifth Avenue, Pittsburgh, PA 15213, USA. e-mail: rojasm@upmc.edu

    Search for more papers by this author

  • No conflicts of interest were declared.

Abstract

The incidence and severity of fibrotic lung diseases increase with age, but very little is known about how age-related changes affect the mechanisms that underlie disease emergence and progression. Normal ageing includes accumulation of DNA mutations, oxidative and cell stresses, mitochondria dysfunction, increased susceptibility to apoptosis, telomere length dysfunction and differential gene expression as a consequence of epigenetic changes and miR regulation. These inevitable ageing-related phenomena may cause dysfunction and impaired repair capacity of lung epithelial cells, fibroblasts and MSCs. As a consequence, the composition of the extracellular matrix changes and the dynamic interaction between cells and their environment is damaged, resulting ultimately in predisposition for several diseases. This review summarizes what is known about age-related molecular changes that are implicated in the pathobiology of lung fibrosis in lung tissue.

Ancillary