Inflamm-aging, that is the age-associated inflammatory status, is considered one of the most striking consequences of immunosenescence, as it is believed to be linked to the majority of age-associated diseases sharing an inflammatory basis. Nevertheless, evidence is emerging that inflamm-aging is at least in part independent from immunological stimuli. Moreover, centenarians who avoided or delayed major inflammatory diseases display markers of inflammation. In this paper we proposed a reappraisal of the concept of inflamm-aging, suggesting that its pathological effects can be independent from the total amount of pro-inflammatory mediators, but they would be rather associated with the anatomical district and type of cells where they are produced and where they primarily act.
Salvioli S., Monti D., Lanzarini C., Conte M., Pirazzini C., Bacalini M.G., et al. (2013). Immune system, cell senescence, aging and longevity - Inflamm-aging reappraised. CURRENT PHARMACEUTICAL DESIGN, 19(9), 1675-1679 [10.2174/1381612811319090015].
Immune system, cell senescence, aging and longevity - Inflamm-aging reappraised.
SALVIOLI, STEFANO;LANZARINI, CATIA;CONTE, MARIA;PIRAZZINI, CHIARA;BACALINI, MARIA GIULIA;GARAGNANI, PAOLO;GIULIANI, CRISTINA;FONTANESI, ELISA;OSTAN, RITA;BUCCI, LAURA;SEVINI, FEDERICA;LUKAS YANI, STELLA;BARBIERI, ANNALAURA;LOMARTIRE, LAURA;BORELLI, VINCENZO;VIANELLO, DARIO;BELLAVISTA, ELENA;MARTUCCI, MORENA;CEVENINI, ELISA;PINI, ELISA;SCURTI, MARIA;BIONDI, FIAMMETTA;SANTORO, AURELIA;CAPRI, MIRIAM;FRANCESCHI, CLAUDIO;Monti, D
2013
Abstract
Inflamm-aging, that is the age-associated inflammatory status, is considered one of the most striking consequences of immunosenescence, as it is believed to be linked to the majority of age-associated diseases sharing an inflammatory basis. Nevertheless, evidence is emerging that inflamm-aging is at least in part independent from immunological stimuli. Moreover, centenarians who avoided or delayed major inflammatory diseases display markers of inflammation. In this paper we proposed a reappraisal of the concept of inflamm-aging, suggesting that its pathological effects can be independent from the total amount of pro-inflammatory mediators, but they would be rather associated with the anatomical district and type of cells where they are produced and where they primarily act.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
