ArticleScience China. Life sciences2025
Altered 3D genome reorganization mediates precocious myeloid differentiation of aged hematopoietic stem cells in inflammation.
Article in Science China. Life sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Aging-associated SATB1 deficiency remodels 3D genome architecture and transcriptional programs in naive CD4Science advances · 2026Article
- Age-related IGF-1 decline permits a redox-sensitive transcriptional shift that directs hematopoiesis toward a CCR2Redox biology · 2026Article
- A new role of iridium(III) complexes in regulating pluripotency acquisition via mitochondrial remodulation.Science China. Life sciences · 2026Article
- P-selectin delineates conserved functional heterogeneity in early hematopoietic stem cell aging in humans and mice.The EMBO journal · 2026Article
- Diabetes Mellitus with Influenza Virus and Subsequent Bacterial Infection: Triple Pathological Interactions and Challenges.International journal of molecular sciences · 2026Review
- Transcriptomic Profiling of Adipose Tissues in Sujiang Pigs Reveals Candidate Genes Associated with Tissue-Specific Fat Deposition.Life (Basel, Switzerland) · 2026Article
- TRIM21 contributes to senile osteoporosis by shifting the osteoadipogenic balance toward adipogenesis in BMSCs.Science China. Life sciences · 2026Article
- Hematopoietic Stem Cell Aging: Mechanisms, Microenvironment Influences, and Rejuvenation Strategies.Bioengineering (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
26 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is a driving force of hematopoietic stem cells (HSCs) aging, causing irreversible exhaustion of functional HSCs. However, the underlying mechanism of HSCs erosion by inflammatory insult remains poorly understood. Here, we find that transient LPS exposure primes aged HSCs to undergo accelerated differentiation at the expense of self-renewal, leading to depletion of HSCs. Meanwhile, the central regulator nuclear factor kappa B (NF-κB) mediating functional impairment by inflammation insult induces differential transcriptional response in aged HSCs compared with young HSCs, with precocious activation of myeloid lineage genes. Altered compartmentalization and chromatin loop formation are associated with aging-related differential transcriptional response in HSCs upon lipopolysaccharide (LPS) stimulation. Mechanistically, enhancer and promoter regions of myeloid lineage genes in aged HSCs are more accessible and display more rapid and prominent CTCF occupancy upon LPS stimulation. Our study provides comprehensive resources for the three-dimensional (3D) genome structure of HSCs and sheds light into the ordered genome organization and the associated transcriptome signature underlying HSCs aging.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.