ArticleMolecular cell2025
Centromere inactivation during aging can be rescued in human cells.
Article in Molecular cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Target identification and assessment in the era of AI.Nature reviews. Drug discovery · 2026Review
- Insights into the therapeutic strategies for aging and aging-associated diseases.Signal transduction and targeted therapy · 2026Review
- Oxidative DNA lesions destabilize centromeres and drive chromosome instability.bioRxiv : the preprint server for biology · 2026Article
- Developmental regulation of kinetochore phosphorylation determines mitotic fidelity.bioRxiv : the preprint server for biology · 2026Article
- Nucleosome spacing across cell types, diseases, and ages.Nucleic acids research · 2026Review
- Oncogenic lncRNA transgene transcription modulates epigenetic memory at a naïve chromosomal locus.Nucleus (Austin, Tex.) · 2025Article
- Robust CENP-A incorporation in human cells is independent of transcription and cohesin components.Molecular biology of the cell · 2025Article
- CENP-A is diluted during bovine spermatogenesis and is maintained at internally positioned centromere clusters in mature bull sperm.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025Article
- Causality of Aging Hallmarks.Aging and disease · 2025Review
- Silencing centromeres with age.Nature reviews. Molecular cell biology · 2025Article
- Introducing Aurora Kinase A as a Gene Target Against Photoaging: A Network Analysis.Journal of lasers in medical sciences · 2025Article
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Abstract
Aging involves a range of genetic, epigenetic, and physiological alterations. A key characteristic of aged cells is the loss of global heterochromatin, accompanied by a reduction in canonical histone levels. In this study, we track the fate of centromeres in aged human fibroblasts and tissues and in various cellular senescent models. Our findings reveal that the centromeric histone H3 variant CENP-A is downregulated in aged cells in a p53-dependent manner. We observe repression of centromeric noncoding transcription through an epigenetic mechanism via recruitment of a lysine-specific demethylase 1 (LSD1/KDM1A) to centromeres. This suppression results in defective de novo CENP-A loading at aging centromeres. By dual inhibition of p53 and LSD1/KDM1A in aged cells, we mitigate the reduction in centromeric proteins and centromeric transcripts, leading to the mitotic rejuvenation of these cells. These results offer insights into a unique mechanism for centromeric inactivation during aging and provide potential strategies to reactivate centromeres.
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