ArticleGenome research2015
H3K4me1 marks DNA regions hypomethylated during aging in human stem and differentiated cells.
Article in Genome research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 78 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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Who cites it
78 citing papers in PubMed, 153 citations in OpenAlex.
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- TRIM37-PARP1-TET1 axis maintains stemness and prevents osteoporosis by inhibiting DNMT1 alternative splicing via 5hmC regulation.Nature communications · 2025Article
- Cellular senescence and other age-related mechanisms in skeletal diseases.Bone research · 2025Review
- A Novel Framework for the Design of Minimized Epigenetic Clocks Using the Analysis of DNA Methylation Heterogeneity.International journal of molecular sciences · 2025Article
- The influence of cell source on the senescence of human mesenchymal stem/stromal cells.Human cell · 2025Review
- Retarding human adipose-derived MSCs senescence and promoting tendon repair using cell sheet engineering with a histone methyltransferase inhibitor.Scientific reports · 2025Article
- Age-related changes in DNA methylation in a sample of elderly Brazilians.Clinical epigenetics · 2025Article
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- Integrative mapping of the dog epigenome: Reference annotation for comparative intertissue and cross-species studies.Science advances · 2023Article
- Impact of Environmental and Epigenetic Changes on Mesenchymal Stem Cells during Aging.International journal of molecular sciences · 2023Review
- Data-driven identification and classification of nonlinear aging patterns reveals the landscape of associations between DNA methylation and aging.Human genomics · 2023Article
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- Utility of DNA Methylation as a Biomarker in Aging and Alzheimer's Disease.Journal of Alzheimer's disease reports · 2023Review
- Epigenetic control of mesenchymal stem cells orchestrates bone regeneration.Frontiers in endocrinology · 2023Review
- Aging and cancer epigenetics: Where do the paths fork?Aging cell · 2022Review
- Bone Marrow Aging and the Leukaemia-Induced Senescence of Mesenchymal Stem/Stromal Cells: Exploring Similarities.Journal of personalized medicine · 2022Review
- Potential pre-activation strategies for improving therapeutic efficacy of mesenchymal stem cells: current status and future prospects.Stem cell research & therapy · 2022Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
30 authors at 12 institutions in 7 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In differentiated cells, aging is associated with hypermethylation of DNA regions enriched in repressive histone post-translational modifications. However, the chromatin marks associated with changes in DNA methylation in adult stem cells during lifetime are still largely unknown. Here, DNA methylation profiling of mesenchymal stem cells (MSCs) obtained from individuals aged 2 to 92 yr identified 18,735 hypermethylated and 45,407 hypomethylated CpG sites associated with aging. As in differentiated cells, hypermethylated sequences were enriched in chromatin repressive marks. Most importantly, hypomethylated CpG sites were strongly enriched in the active chromatin mark H3K4me1 in stem and differentiated cells, suggesting this is a cell type-independent chromatin signature of DNA hypomethylation during aging. Analysis of scedasticity showed that interindividual variability of DNA methylation increased during aging in MSCs and differentiated cells, providing a new avenue for the identification of DNA methylation changes over time. DNA methylation profiling of genetically identical individuals showed that both the tendency of DNA methylation changes and scedasticity depended on nongenetic as well as genetic factors. Our results indicate that the dynamics of DNA methylation during aging depend on a complex mixture of factors that include the DNA sequence, cell type, and chromatin context involved and that, depending on the locus, the changes can be modulated by genetic and/or external factors.
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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.