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.
Inflamm-aging of the stem cell niche: Breast cancer as a paradigmatic example: Breakdown of the multi-shell cytokine network fuels cancer in aged people / Bonafè M.; Storci G.; Franceschi C.. - In: BIOESSAYS. - ISSN 0265-9247. - STAMPA. - 34:(2012), pp. 40-49. [10.1002/bies.201100104]
Inflamm-aging of the stem cell niche: Breast cancer as a paradigmatic example: Breakdown of the multi-shell cytokine network fuels cancer in aged people.
BONAFE', MASSIMILIANO;STORCI, GIANLUCA;FRANCESCHI, CLAUDIO
2012
Abstract
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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.