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Óðrmaxxing
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Article is very long and graphs and data are confuseing to interpret, so i write summary of the data (kept to the minimum simplicity while conveying all the most interesting info) . the takeaway is that longevity mechanisms of long lived species are separate from those used to extend lifespan of lab mice .
Greater MPG (DNA-3-methyladenine glycosylase) and RPL28 are associated with greater maximum lifespan across mammalian taxonomic orders while the opposite is true for Cul4b. RPL28 and RPL30 were associated also with greater time to female maturity, with this correlation even stronger than that on maximum lifespan. Cul4b expression was correlated with quicker female maturity. Sdc1 (in kidney), Hebp2 (in liver), Npm2 (in brain), Tnip1 (in liver) expression was associated with species maximum lifespan, while the reverse was true for Adprh (brain), Dtl (Denticleless E3 Ubiquitin Protein Ligase Homolog, brain), Slc22a8 (brain), Stxbp5 (kidney). With ageing, Vsig4 was upregulated and Nrep (neuronal regeneration related protein/Neuronal protein 3.1) was downregulated. IGF1 expression was slightly negatively correlated with species longevity but also ageing, and more strongly correlated with pro-longevity interventions (data on interventions in mice). Mrps15 expression was positively correlated with species longevity and pro-longevity interventions and downregulated with ageing. Ndufa9 expression was correlated with pro-longevity interventions but oddly negatively correlated with species longevity and was downregulated with age. Lgals1 was positively correlated with species longevity and pro-longevity interventions but also increased during ageing. Rela (p65) was mildly correlated with species longevity but decreased with pro-longevity interventions, while it increased with age. C1qb was mildy correlated with species longevity but mildly decreased with pro-longevity interventions, yet strongly increased with ageing.
Uric acid concentrations decreaded with pro-longevity interventions but increased with species longevity. Allantoin barely increased (results mixed of increased, decreased, and insignificant change) yet decreased with species longevity. NAD+ increased with pro longevity interventions but had mixed results (differed by organ) with species longevity. L-crystathionine decreased with pro longevity interventions except for rapamycin (M & F) and CR male mice, where it was unchanged but had mixed results (differed by organ) with species longevity. Uox (Urate oxidase) decreased with species longevity but increased with longevity interventions. Nadsyn1 increased with both species maximum lifespan and longevity interventions. Cth (cystathionine gamma-lyase) decreased with species longevity but increased with longevity interventions.
Cardamonin aided survival of fibroblasts after paraquat-induced oxidative stress from short lived species but not long-lived species, whilst clofilium tysolate and deguelin benefited the surival in both short and long lived species, at least in terms of the trend; there were a few exceptions of a neutral effect. Importantly, clofilium tysolate and deguelin but not cardamonin benefited human fibroblast survival.
