Untitled research work

Primary cellular proteostatic mechanisms within mice. Multiple components of the proteostatic network are known to be deleteriously affected by ageing but such age-associated changes may be slowed and/or delayed in long-lived mice. Consequently, it has been suggested that the ability to better maintain proteostasis over the life-course underlies both the greater lifespan and healthspan of long-lived mutant mice. UPRER, endoplasmic reticulum stress unfolded protein response; UPRmt, mitochondrial unfolded protein response; ERAD, endoplasmic reticulum associated protein degradation.