Autophagy is increasingly thought to play an important role in aging, in part because autophagic degradation allows cells to prevent the accumulation of damaged macromolecules such as oxidized proteins and advanced glycation endproducts (AGEs).

I’ve been slowly squirreling away abstracts about the subject, and they’ve been building up — so on this crisp nearly-winter day I figured that it might be time to dig up some of those nuts:

  • In heart muscle, calorie restriction (CR) boosts autophagy, both by increasing the number of autophagosomes and the expression of autophagy-related proteins. Wohlgemuth et al. suggest that this might provide a mechanism for the beneficial effects of CR on cardiac tissue.
  • The overall rate of autophagy decreases with age. One specific flavor of degradation that undergoes such a decline is chaperone-mediated autophagy, which directs cytosolic proteins to the lysosome via an interaction with an intracellular receptor. Kiffin et al. have tracked down the cause of this decline, and lay the blame on changes in the processing and stability of the lysosomal receptor LAMP-2.
  • The benefits of autophagy (and the hazards resulting from its age-related decline) are hinted at in the results of Bergamini et al., who show that an anti-lipolytic drug that stimulates autophagy can reverse at least one biomarker of aging, in this case high levels of altered mitochondrial DNA. The authors also address the relationship between CR and the cellular adaptation to fasting, and argue that autophagy is essential to the anti-aging action of CR.