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[ImmInst]

Artificial blood: the quest for one of science's holy grails http://buff.ly/2lYytla 

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[alc]

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As somatic cell reprogramming, as here, mediates an epigenetic ‘reset’ of the parental cells, but should leave any underlying DNA mutations unrepaired, our results fail to support the view that accumulations of DNA mutations in genes critical for haematopoiesis would be the principal/only mechanism for aged-dependent functional decline of HSCs. Instead, our results favour an altered epigenome to be a major contributor to HSC ageing. This does not exclude that mechanisms involving macromolecular damage/insult might contribute to other aspects of HSC ageing not approached here. For instance, the nature of our experiments does not allow us to assess age-induced changes that lead to a direct cellular loss. At the same time, the aged epigenome can still be strongly rooted, which is not least supported by the recent data, suggesting that direct conversion of aged fibroblasts into neurons rendered cells with a retained aged transcriptome Therefore, a rather complete epigenomic ‘reset’, like that shown here, might be needed to normalize the alterations that arise and govern cellular ageing. While it remains to be determined how this could be achieved in a more tractable manner, we believe our results should be encouraging for the prospects of such efforts, which in the long term would pave the way for the development of therapeutic modalities aimed at achieving overall healthier late stages of life.

 

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