ArticleCell stem cell2013
Proliferation-dependent alterations of the DNA methylation landscape underlie hematopoietic stem cell aging.
Article in Cell stem cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 293 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.
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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
293 citing papers in PubMed, 476 citations in OpenAlex.
- Cell-type specific impact of metformin on monocyte epigenetic age reversal in virally suppressed older people living with HIV.Aging cell · 2024Trial
- Hematopoietic Stem Cell Metabolism during Stress and Aging.Advances in geriatric medicine and research · 2026Article
- Epigenetics in development, disease, and therapy: from mechanisms to clinical interventions.Science China. Life sciences · 2026Review
- Geneformer-guided multiomics integration identifies Pbx1 as a network hub of hematopoietic stem cell aging.Science advances · 2026Article
- Stem cells as an essential mediator of the exercise-tumorigenesis link.Nature reviews. Cancer · 2026Review
- Single-Cell Analyses Reveal Dysregulation of Ribosomal Protein Genes During Hematopoietic Stem and Progenitor Cell Aging.Advanced biology · 2026Article
- Hematopoietic stem cell aging: a review of transcriptional and multi-omics insights and potential paths for AI integration.Experimental & molecular medicine · 2026Review
- Loss of tissue-state plasticity: a conceptual framework for age-associated regenerative failure.Inflammation and regeneration · 2026Review
- Developmental timing distinguishes pediatric and adult cancers through retention and rewiring mechanisms.Nature communications · 2026Review
- A progeria syndrome links DNA hypermethylation to age-related pathology.Nature genetics · 2026Article
- Immune aging biomarkers for clinical trials.Nature medicine · 2026Review
- Architectural fragility of gene regulatory networks underlies hematopoietic stem cell aging.bioRxiv : the preprint server for biology · 2026Article
- Aging mechanisms and rejuvenation strategies for hematopoietic stem cells.Genome biology · 2026Review
- From complexity to clarity: aging bone marrow niche in bone and blood regeneration and malignancy.Bone research · 2026Review
- Transposable elements in hematopoietic stem cells upon aging and myeloid malignancies.Mobile DNA · 2026Review
- Non-necroptotic MLKL function damages mitochondria and promotes hematopoietic stem cell aging.Nature communications · 2026Article
- Age-Like Methylation Changes of HSCs in GADD45B Knockout Mice Define Methylation Sites Associated With Loss of Function.Aging cell · 2026Article
- Metabolic and epigenetic interplay in HSPC specification: A balance between extrinsic and intrinsic cues.iScience · 2026Review
- Chromatin reorganization drives overexpression of a Btaf1 variant underpinning hematopoietic aging.Nature communications · 2026Article
- "Metabolic memory" of aging: anchoring, transmission, and frontiers of transgenerational intervention.Biogerontology · 2026Review
233 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The functional potential of hematopoietic stem cells (HSCs) declines during aging, and in doing so, significantly contributes to hematopoietic pathophysiology in the elderly. To explore the relationship between age-associated HSC decline and the epigenome, we examined global DNA methylation of HSCs during ontogeny in combination with functional analysis. Although the DNA methylome is generally stable during aging, site-specific alterations of DNA methylation occur at genomic regions associated with hematopoietic lineage potential and selectively target genes expressed in downstream progenitor and effector cells. We found that age-associated HSC decline, replicative limits, and DNA methylation are largely dependent on the proliferative history of HSCs, yet appear to be telomere-length independent. Physiological aging and experimentally enforced proliferation of HSCs both led to DNA hypermethylation of genes regulated by Polycomb Repressive Complex 2. Our results provide evidence that epigenomic alterations of the DNA methylation landscape contribute to the functional decline of HSCs during aging.
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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.