The aging process jeopardizes the maintenance of cellular homeostasis leading to the activation of a variety of host defence systems. Inflammasomes are intracellular multiprotein sensors which can recognize a large set of danger signals, induced either by pathogens or cellular stress, and once activated, they subsequently stimulate inflammatory responses [15-18]. There are several subfamilies of NOD-like receptors (NLR) but emerging data indicates that the NLRP subfamily, in particular the NLRP3 member, is the major sensor for “intracellular danger-associated molecular patterns” (DAMPs). Inflammasomes are signaling platforms which are assembled after the recognition of DAMP by the receptor protein. In the case of NLRP3, the activated receptor interacts with the adaptor protein ASC which recruits the inflammatory caspase-1 (CASP-1) to the complex which subsequently oligomerizes into penta- or heptameric inflammasomes [16,19]. CASP-1 is the common effector molecule in inflammasomes which cleaves the inactive precursors of two proinflammatory cytokines, i.e. IL-1β and IL-18, into their mature forms which are then secreted from cells. In addition to CASP-1, some other inflammatory caspases, e.g. CASP-4, CASP-5 and CASP-12, can also process the proforms of these
