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The NADase CD38 is induced by factors secreted from senescent cells providing a potential link between senescence and age-related cellular NAD+ decline.

Ever since I learned that CD38 expression seems upregulated with aging, and its activity seems to be an important cause of the age-related decline in NAD+ with age, I have wondered: why does CD38 get upregulated? This study may have an answer to this question. This group reports that SASP factors secreted by senescent cells can upregulate CD38 in non-senescent cells. So one might suspect that serum NAD+ would increase after a round of senolytic treatment. I wonder whether anyone has assessed for that potential outcome after senolytics.
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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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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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Activation of the mTORC1/PGC-1 axis promotes mitochondrial biogenesis and induces cellular senescence in the lung epithelium.

Perhaps I missed this association in my PubMed screening, but I don't think I've heard of this association between cellular senescence and increased mitochondrial biogenesis. I assumed increased mitochondrial biogenesis was almost unconditionally a good thing, but this group reports that it occurs in senescent lung epithelial cells. I wonder: could this increased biogenesis be caused by a reduction in ATP availability experienced by the senescent cell? I presume that would be a normal signal for increased mitochondrial biogenesis (a decline in ATP or an increase in AMP), but I'm not well-read on this subject.
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