Inflamm-aging, cytokines and aging: state of the art, new hypotheses on the role of mitochondria and new perspectives from systems biology.
In this article we summarise present knowledge on the role of pro-inflammatory cytokines on chronic inflammation leading to organismal aging, a phenomenon we proposed to call "inflamm-aging". In particular, we review genetic data regarding polymorphisms of genes encoding for cytokines and proteins involved in natural immunity (such as Toll-like Receptors and Heat Shock Proteins) obtained from large population studies including young, old and very old people in good health status or affected by age-related diseases such as Alzheimer's Disease and Type II Diabetes. On the whole, despite some controversial results, the available data are in favour of the hypothesis that pro-inflammatory cytokines play an important role in aging and longevity. Further, we present a possible hypothesis to reconcile energetic dysfunction, including mitochondria, and inflamm-aging. New perspectives for future studies, including phylogenetic studies in animal models and in silico studies on mathematical and bioinformatic models inspired by the systems biology approach, are also proposed.
Salvioli
S
S
Department of Experimental Pathology, University of Bologna, via S. Giacomo 12, Bologna, Italy. stefano.salvioli2@unibo.it
Capri
M
M
Valensin
S
S
Tieri
P
P
Monti
D
D
Ottaviani
E
E
Franceschi
C
C
D000375:Aging / Q000502:physiology*; D000818:Animals; D016207:Cytokines / Q000235:genetics / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000503:physiopathology*; D008928:Mitochondria / Q000502:physiology*; D010802:Phylogeny; D011110:Polymorphism, Genetic / Q000235:genetics; D049490:Systems Biology / Q000379:methods
D016207:Cytokines