Researcher have been examining the role of NF-κB in accelerated aging conditions such as Hutchinson-Gilford Progeria Syndrome, and believe that the findings may also be relevant as a basis for therapies to slow the ordinary progression of degenerative aging:
NF-κB transcription factors respond to a large variety of external and internal stress signals, having essential roles in development and tissue https://en.wikipedia.org/wiki/Homeostasis>homeostasis maintenance. The in vivo monitoring of NF-κB activity by using a reporter-based assay revealed that this pathway was constitutively hyperactivated in progeroid mice. Further experiments allowed us to unveil the molecular pathway involved in this aberrant activation.
[Our] results indicate that these findings can be extended to normal aging, suggesting that a common accumulation of genetic damage and nuclear envelope alterations with age could be responsible, at least in part, of the abnormal NF-κB activity reported in tissues from advanced aged donors. The accumulation of senescent cells together with the decline in adult stem cell function is a primary cause of the compromise of tissue homeostasis during aging. The primary function of NF-κB activation in this context could be related to the prevention of apoptosis of damaged cells, so that chronic activation of this pathway with the subsequent immunological decline could preclude a proper clearance of senescent and damaged cells.
[Experimental data] confirm that NF-κB signaling is active during normal aging, its hyperactivation is associated with the development of accelerated aging and its amelioration retards the aging process. These characteristics support the use of strategies aimed at controlling NF-κB related inflammation as putative rejuvenation strategies during both normal and pathological aging.