No conflicts of interest were declared.
Influence of age on wound healing and fibrosis
Article first published online: 12 DEC 2012
Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
The Journal of Pathology
Volume 229, Issue 2, pages 310–322, January 2013
How to Cite
Kapetanaki, M. G., Mora, A. L. and Rojas, M. (2013), Influence of age on wound healing and fibrosis. J. Pathol., 229: 310–322. doi: 10.1002/path.4122
- Issue published online: 12 DEC 2012
- Article first published online: 12 DEC 2012
- Accepted manuscript online: 1 NOV 2012 09:09AM EST
- Manuscript Accepted: 2 OCT 2012
- Manuscript Revised: 30 SEP 2012
- Manuscript Received: 3 SEP 2012
- lung fibrosis;
- extracellular matrix;
- chronic obstructive pulmonary disease
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.