ArticleNature communications2026
Epigenetic profiling of hematopoietic stem cells from male mice identifies KDR and PU.1 as regulators of aging transcriptome and caloric restriction response.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Review
- Hematopoietic stem cell aging: a review of transcriptional and multi-omics insights and potential paths for AI integration.Experimental & molecular medicine · 2026Review
- Chromatin reorganization drives overexpression of a Btaf1 variant underpinning hematopoietic aging.Nature communications · 2026Article
- Epigenetic profiling of hematopoietic stem cells from male mice identifies KDR and PU.1 as regulators of aging transcriptome and caloric restriction response.Nature communications · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Caloric restriction (CR) provides anti-aging benefits but has also been reported to be associated with reduced immune function, and how hematopoietic stem cells (HSCs) potentially contribute to this decline remains unclear. Using lifelong and short-term CR in male mice, we found reducing the energy supply decreases total white blood cell production and shifts hematopoiesis towards myeloid and thrombo-erythroid lineages, prioritizing cells essential for survival (red blood cells, platelets, innate immune cells) over adaptive immunity. HSCs under CR enter cell cycle to support myeloid differentiation rather than self-renewal. Lifelong CR inhibits age-associated transcriptome changes in HSCs, though age-associated profiles appear shortly after ad libitum feeding. Epigenetic profiling identified KDR as a key CR response regulator, and Kdr knockdown in aged HSCs recapitulated the youthful transcriptome of lifelong CR HSCs. Finally, we show PU.1 acts as an intracellular regulator of CR response, controlling HSC self-renewal and differentiation through increased target gene binding under CR conditions.
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Registered trials
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