Journal
BIOESSAYS
Volume 34, Issue 1, Pages 40-49Publisher
WILEY
DOI: 10.1002/bies.201100104
Keywords
ageing; cancer; DNA damage; inflammation; stem cell; stem cell niche
Categories
Funding
- EU [223576, 200880, 266486]
- Italian Ministry of University and Research
- Cornelia-Roberto Pallotti Foundation
- [PRIN 2008KTRN38]
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Inflamm-aging is a relatively new terminology used to describe the age-related increase in the systemic pro-inflammatory status of humans. Here, we represent inflamm-aging as a breakdown in the multi-shell cytokine network, in which stem cells and stromal fibroblasts (referred to as the stem cell niche) become pro-inflammatory cytokine over-expressing cells due to the accumulation of DNA damage. Inflamm-aging self-propagates owing to the capability of pro-inflammatory cytokines to ignite the DNA-damage response in other cells surrounding DNA-damaged cells. Macrophages, the major cellular player in inflamm-aging, amplify the phenomenon, by broadcasting pro-inflammatory signals at both local and systemic levels. On the basis of this, we propose that inflamm-aging is a major contributor to the increase in cancer incidence and progression in aged people. Breast cancer will be presented as a paradigmatic example for this relationship.
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