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. 2021 May 11;12:2665. doi: 10.1038/s41467-021-22863-0

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Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — With age, HSC undergo several changes including expansion of the stem cell pool, reduction in homing and engraftment potential and myeloid biased differentiation. These functional changes are associated with reduced Sirt3 expression and reduced mitophagy with a concomitant increase in the mitochondrial network and increased metabolism that is reliant on oxidative phosphorylation. These changes are underpinned by the altered transcriptional programme of aged HSC. Repletion of the age-associated decrease in NAD levels in HSC via nicotinamide riboside (NR) results in a reduction of the HSC pool as well as changes in the transcriptional programme of aged HSC towards a “more youthful” state and is associated with improved engraftment and partial reversion of the myeloid bias following transplantation of HSC isolated from NR-treated aged mice. These effects may be driven by increased Sirt3 expression, reduced levels of Hspa1a and decreased metabolism through oxidative phosphorylation as well as increased mitophagy, which results in a reduction of mitochondrial network and output.