There are several regulatory mechanisms which could augment the appearance of inflammaging phenotype during the age-related deficiency of autophagy. It is well-known that increased levels of ROS can activate NF-κB signaling via multiple mechanisms [92-94]. For instance, several redox-sensitive protein kinases and phosphatases can stimulate IKK-NF-κB signaling and thus induce and maintain an elevated priming state of inflammasomal system. Moreover, a decline in autophagy can stimulate the activating kinases of the NF-κB complex, i.e. IκB kinase α and β (IKKα/β) and NF-κB-inducing kinase (NIK), which are degraded via selective autophagy [95-97]. Sequestosome-1/p62 is a cargo receptor for selective autophagy [98] and changes in autophagy regulate the p62 level which controls the formation of protein aggregates as well as activation of NF-κB signaling [99,100]. Both of these responses are typical hallmarks of inflammaging and inducers of inflammasomes.
