ArticleeLife2025
Alteration of long- and short-term hematopoietic stem cell ratio causes myeloid-biased hematopoiesis.
Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- ANGPTL8 induces the aging of hematopoietic stem/progenitor cells.Biogerontology · 2026Article
- Improving lymphopoiesis in aged bone marrow.Current opinion in hematology · 2026Review
- Longevity through immunity: the unusual naked mole-rat immune system.GeroScience · 2026Review
- Article
- Single-cell integration analysis reveals molecular signatures of the tumor microenvironment in early-onset colorectal cancer.NPJ precision oncology · 2025Article
- Ageing, immune fitness and cancer.Nature reviews. Cancer · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
Myeloid-biased hematopoiesis is a well-known age-related alteration. Several possibilities, including myeloid-biased hematopoietic stem cell (HSC) clones, may explain this. However, the precise mechanisms remain controversial. Utilizing the Hoxb5 reporter system to prospectively isolate long-term HSCs (LT-HSCs) and short-term HSCs (ST-HSCs), we found that young and aged LT-HSCs co-transplanted into the same recipients demonstrated nearly equivalent myeloid lineage output, contrary to the theory of myeloid-biased HSC clones. Transcriptomics indicated no significant myeloid gene enrichment in aged LT-HSCs compared to their young counterparts. Instead, transplanting reconstituted young HSCs with the ratio of LT/ST-HSCs seen in aged mice can significantly skew the lineage output to myeloid cells. In addition, while the niche environment in the bone marrow minimally affects myeloid-biased hematopoiesis, aged thymi and spleens substantially hinder lymphoid hematopoiesis, resulting in further myeloid domination. Thus, we demonstrate that myeloid-biased hematopoiesis in aged mice originates due to alteration of the ratio between LT-HSCs and ST-HSCs rather than in heterogeneous HSC clones with various cell fates.
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Registered trials
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