A typical feature of ageing is a chronic, low-grade inflammation characterized by a general increase in the production of proinflammatory
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 presente