ArticleCell death & disease2025
P-selectin overexpression impairs hematopoietic stem cell homeostasis via inflammatory receptor-mediated proliferation and differentiation.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Senescence-directed nanotherapy ameliorates fibrosis and overcomes immune exclusion in cancer.Science (New York, N.Y.) · 2026Article
- P-selectin delineates conserved functional heterogeneity in early hematopoietic stem cell aging in humans and mice.The EMBO journal · 2026Article
- Hematopoietic stem cell aging: a review of transcriptional and multi-omics insights and potential paths for AI integration.Experimental & molecular medicine · 2026Review
- Improving lymphopoiesis in aged bone marrow.Current opinion in hematology · 2026Review
- Cell surface RNAs define a new interface for immune recognition.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Hematopoietic stem cells (HSC) sustain lifelong blood and immune system homeostasis. This study identifies P-selectin as a pivotal regulator of HSC function under aging and inflammatory stress. We observed pronounced Selp upregulation in aged HSC and inflammatory contexts, which drives excessive proliferation and differentiation while depleting their long-term self-renewal capacity. Using tissue-specific Selp overexpression models, we demonstrate that chronic Selp elevation disrupts HSC polarity, promotes oxidative stress accumulation, and induces genomic instability. Over time, sustained Selp expression leading to LT-HSC exhaustion and impaired hematopoietic reconstitution. Single-cell transcriptomics revealed that Selp enforces a pro-inflammatory transcriptional program in HSC, hyperactivating IFN-γ and PI3K-AKT-MOTR signaling pathways. Mechanistically, P-selectin directly interacted with IFNγR1 on the HSC surface, which driving activation of JAK1-STAT1 and PI3K-AKT-mTOR signaling axes. Notably, Selp overexpression suppresses the pathogenic capacity of leukemia stem cells (LSC), highlighting potential therapeutic implications. Our findings established P-selectin as a molecular nexus linking chronic inflammation and aging to hematopoietic decline, with dual therapeutic implications: targeting P-selectin may mitigate age-related hematopoietic dysfunction while offering a strategy to selectively impair LSC activity in malignancies.
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Registered trials
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