This suggests that rDNA is the more common lifespan determinant.
A longitudinal repeated measures design over pregnancy and post-birth, with a control group would provide insight into the mechanical adaptations of the body under conditions of changing load during a common female human lifespan condition, while minimizing the influences of inter human differences.
Thus, nhr-49-mediated metabolic reprogramming-induced longevity is a common mechanism for lifespan extension during DR. DR is known to produce reduced levels of ROS, potent oxidizing agents that damage cellular macromolecules and may be the underlying cause of aging (Pamplona & Barja, 2007; Page et al., 2010).
Thus, our findings suggest that autophagy induction is a common requirement for lifespan-prolonging measures, while they underscore the importance of autophagy as a protective (rather than destructive) phenomenon.
For example, in yeast, CR and numerous low-intensity stressors associated with longevity activate a common pathway to influence lifespan (Anderson et al., 2003).
Whether the different methods of restricting nutrients converge on a common pathway to extend lifespan or whether independent mechanisms are elicited depending on how DR is achieved is still unclear.
Seemingly, clearing cellular damage by autophagy is a common denominator of many lifespan-extending manipulations [ 91].
Together, these results are consistent with the idea that DAGL/ inaE and rdgA modulate lifespan via a common pathway.
This epistatic analysis suggests that SIR-2.1 accumulation and CEP-1 depletion extend lifespan through a common final pathway that relies on the induction of autophagy.
Furthermore, the regulation of both paraquat resistance and lifespan by a common genetic pathway suggests that these two phenotypes are physiologically interdependent.
