Influence of age on wound healing and fibrosis

J Pathol. 2013 Jan;229(2):310-22. doi: 10.1002/path.4122.


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.

Publication types

  • Review

MeSH terms

  • Age Factors
  • Aging / genetics
  • Aging / metabolism
  • Aging / pathology*
  • Animals
  • Apoptosis
  • Epigenesis, Genetic
  • Epithelial Cells / metabolism
  • Epithelial Cells / pathology
  • Extracellular Matrix / metabolism
  • Extracellular Matrix / pathology
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Fibrosis
  • Humans
  • Lung / metabolism
  • Lung / pathology*
  • Mesenchymal Stem Cells / metabolism
  • Mesenchymal Stem Cells / pathology
  • Pulmonary Fibrosis / genetics
  • Pulmonary Fibrosis / metabolism
  • Pulmonary Fibrosis / pathology*
  • Telomere / metabolism
  • Wound Healing* / genetics