The epigenetics of inflammaging: The contribution of age-related heterochromatin loss and locus-specific remodelling and the modulation by environmental stimuli

•Epigenetic markers record inflammaging sources during the life course.•A reciprocal relationship between epigenetics and inflammaging exists.•Age-associated epigenetic changes can contribute to inflammaging.•Specific, although limited, epigenetic signatures of inflammaging also exist.•The environment can modulate the relationship between epigenetics and inflammaging. A growing amount of evidences indicates that inflammaging – the chronic, low grade inflammation state characteristic of the elderly – is the result of genetic as well as environmental or stochastic factors. Some of these, such as the accumulation of senescent cells that are persistent during aging or accompany its progression, seem to be sufficient to initiate the aging process and to fuel it. Others, like exposure to environmental compounds or infections, are temporary and resolve within a (relatively) short time. In both cases, however, a cellular memory of the event can be established by means of epigenetic modulation of the genome. In this review we will specifically discuss the relationship between epigenetics and inflammaging. In particular, we will show how age-associated epigenetic modifications concerned with heterochromatin loss and gene-specific remodelling, can promote inflammaging. Furthermore, we will recall how the exposure to specific nutritional, environmental and microbial stimuli can affect the rate of inflammaging through epigenetic mechanisms, touching also on the recent insight given by the concept of trained immunity.