ArticleAging cell2023
Young donor hematopoietic stem cells revitalize aged or damaged bone marrow niche by transdifferentiating into functional niche cells.
Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Single-Cell Profiling Reveals RAB13Aging cell · 2026Article
- Cerebral organoid exosomes reversed behavioral deficits by repressing NLRP3-mediated neuroinflammation in stress models.iScience · 2026Article
- Phenotypic Aging and Sexual Dimorphism in C57BL/6J, SAMR1, and SAMP8 Mice: A Comparative Study.Mediators of inflammation · 2026Article
- Hematopoietic Stem Cell Aging: Mechanisms, Microenvironment Influences, and Rejuvenation Strategies.Bioengineering (Basel, Switzerland) · 2025Review
- Targeting immunosenescence and inflammaging: advancing longevity research.Experimental & molecular medicine · 2025Review
- A Study of Skeletal Stem Cell Dynamics and Its Potential Applications in the Design of a Titanium Implant for Senile Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Stem Cell Niche Concept: Search for Current Expert Consensus.International journal of molecular sciences · 2025Review
- The role of the haematopoietic stem cell niche in development and ageing.Nature reviews. Molecular cell biology · 2025Review
- Endothelial heterogeneity in bone marrow: insights across development, adult life and leukemia.Leukemia · 2025Review
- Homing and Engraftment of Hematopoietic Stem Cells Following Transplantation: A Pre-Clinical Perspective.Current oncology (Toronto, Ont.) · 2024Review
- Young donor hematopoietic stem cells revitalize aged or damaged bone marrow niche by transdifferentiating into functional niche cells.Aging cell · 2023Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The bone marrow niche maintains hematopoietic stem cell (HSC) homeostasis and declines in function in the physiologically aging population and in patients with hematological malignancies. A fundamental question is now whether and how HSCs are able to renew or repair their niche. Here, we show that disabling HSCs based on disrupting autophagy accelerated niche aging in mice, whereas transplantation of young, but not aged or impaired, donor HSCs normalized niche cell populations and restored niche factors in host mice carrying an artificially harassed niche and in physiologically aged host mice, as well as in leukemia patients. Mechanistically, HSCs, identified using a donor lineage fluorescence-tracing system, transdifferentiate in an autophagy-dependent manner into functional niche cells in the host that include mesenchymal stromal cells and endothelial cells, previously regarded as "nonhematopoietic" sources. Our findings thus identify young donor HSCs as a primary parental source of the niche, thereby suggesting a clinical solution to revitalizing aged or damaged bone marrow hematopoietic niche.
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