TY - JOUR
T1 - Age-related inflammation
T2 - The contribution of different organs, tissues and systems. How to face it for therapeutic approaches
AU - Cevenini, E.
AU - Caruso, C.
AU - Candore, G.
AU - Capri, M.
AU - Nuzzo, D.
AU - Duro, G.
AU - Rizzo, C.
AU - Colonna-Romano, G.
AU - Lio, D.
AU - Di Carlo, D.
AU - Palmas, M. G.
AU - Scurti, M.
AU - Pini, E.
AU - Franceschi, C.
AU - Vasto, S.
PY - 2010
Y1 - 2010
N2 - A typical feature of ageing is a chronic, low-grade inflammation characterized by a general increase in the production of pro-inflammatory cytokines and inflammatory markers ("inflamm-ageing"). This status may slowly damage one or several organs, especially when unfavorable genetic polymorphisms and epigenetic alterations are concomitant, leading to an increased risk of frailty together with the onset of age-related chronic diseases. The contribution of different tissues (adipose tissue, muscle), organs (brain, liver), immune system and ecosystems (gut microbiota) to age-related inflammation ("inflamm-ageing") will be discussed in this review in the context of its onset/progression leading to site-restricted and systemic effects. Moreover, some of the possible strategies and therapies to counteract the different sources of molecular mediators which lead to the age-related inflammatory phenotype will be presented.
AB - A typical feature of ageing is a chronic, low-grade inflammation characterized by a general increase in the production of pro-inflammatory cytokines and inflammatory markers ("inflamm-ageing"). This status may slowly damage one or several organs, especially when unfavorable genetic polymorphisms and epigenetic alterations are concomitant, leading to an increased risk of frailty together with the onset of age-related chronic diseases. The contribution of different tissues (adipose tissue, muscle), organs (brain, liver), immune system and ecosystems (gut microbiota) to age-related inflammation ("inflamm-ageing") will be discussed in this review in the context of its onset/progression leading to site-restricted and systemic effects. Moreover, some of the possible strategies and therapies to counteract the different sources of molecular mediators which lead to the age-related inflammatory phenotype will be presented.
KW - Age-related diseases
KW - Ageing
KW - Immunosenescence
KW - Inflammation
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U2 - 10.2174/138161210790883840
DO - 10.2174/138161210790883840
M3 - Article
C2 - 20388071
AN - SCOPUS:77950199929
VL - 16
SP - 609
EP - 618
JO - Current Pharmaceutical Design
JF - Current Pharmaceutical Design
SN - 1381-6128
IS - 6
ER -