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Muscle-derived miR-34a increases with age in circulating extracellular vesicles and induces senescence of bone marrow stem cells.

I'm not confident that this particular set of observations will be wildly useful in understanding and addressing cellular senescence, but I'm including it just in case. This group reported that extracellular vesicles enriched for miR-34a could decrease the viability of bone marrow MSC and increase their senescence. Overexpression of miR-34a in extracellular vesicles could also home to bone in vivo and induce senescence there. But tinkering with levels of miR-34a seems like messing with metabolism in a way that can become extremely complex and cumbersome.
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Independent Roles of Estrogen Deficiency and Cellular Senescence in the Pathogenesis of Osteoporosis: Evidence in Young Adult Mice and Older Humans.

This group reports on a series of experiments intended to make a distinction between the negative effects of cellular senescence on bone health, from the negative effects of a lack of estrogen on bone health. They conclude from these experiments in mice that estrogen deficiency seems to have a negative effect on bone health that is independent of age-related cellular senescence.
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Exercise-induced AMPK activation is involved in delay of skeletal muscle senescence.

This group reported some associations between AMPK activation and what appeared to be prevention or reversal of cellular senescence. I found the exercise part of this study particularly interesting: treadmill exercise in mice reduced p16 and p21 expression in older sedentary mice. Could this be representative of a reversal of senescence? If so, how might it be recapitulated in other tissue types? In response to a similar study I reported on, if I recall correctly, Aubrey mentioned that exercise reducing/reversing senescence was not surprising because exercise would help nutrient uptake. If that's true, I wonder whether other tissues (e.g. skin) might experience increased senescence because of relatively poor nutrient uptake (perhaps after adolescence when growth factors that facilitate nutrient uptake decline). For example, I have yet to figure out how to flex my skin (to improve nutrient uptake)! Aubrey and others, what do you think of this concept?
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NAD+ supplementation rejuvenates aged gut adult stem cells.

This group reported that nicotinamide riboside could "rejuvenate" intestinal stem cells from aged mice and "reverses an impaired ability to repair gut damage". Interestingly, it appears that mTORC1 inhibition (via rapamycin administration) could prevent this effect, suggesting that NAD+ restoration may work through increased mTORC1 activity to restore some tissues.
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