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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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Topical applications of an emollient reduce circulating pro-inflammatory cytokine levels in chronically aged humans: a pilot clinical study.

I found this study interesting: topical application of an emollient to the skin (i.e. applying lotion) "normalized" several * systemic* inflammatory factors such as IL-6 in older humans. This makes me wonder: how much of the increase in circulating inflammatory factors during aging could be caused by dysfunctional, damaged, or senescent skin? I wonder how long this reduction of inflammation persisted after the application of emollient.
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MicroRNA-570 is a novel regulator of cellular senescence and inflammaging.

These experiments were done in cell culture but look potentially interesting. This group reports that inhibiting microRNA 570-3p (miR-570-3p) "reverses cellular senescence by restoring sirtuin-1", as well as "suppresses markers of cellular senescence (p16, p21, p27)...restoring cellular growth by allowing progression through the cell cycle". Inhibiting this microRNA also apparently inhibited some SASP factors. Can we learn something useful from the effects of this miRNA?
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