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. Author manuscript; available in PMC: 2017 Mar 1.
Published in final edited form as: Drugs. 2016 Mar;76(3):291–300. doi: 10.1007/s40265-015-0523-6

Figure 1. Proposed mechanisms for the predilection of fibrosis with aging.

Figure 1

Aging may result in “immunosenescence” that results in impaired antigen clearance and autoimmunity; additionally, senescence of epithelial cells and fibroblasts result in impaired regeneration and aberrant recapitulation of developmental genes. These processes may perpetuate epithelial injury/apoptosis and fibroblast activation that results in failed re-epithelialization, fibroblast persistence and progressive fibrosis.