ArticleNAR molecular medicine2025
Active chromatin marks and up-regulation of FOXC1 in uterine epithelial cells demarcate the onset of reproductive decline in aging females.
Article in NAR molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- The imprinted Peg3 gene is a potent regulator of the DNA methylome in trophoblast cells.Stem cell reports · 2026Article
- Advancing Human Placental Modeling Through Stem-Cell-Derived Trophoblast Organoids and Reprogramming Innovations.Biomedicines · 2026Review
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Authors and funding
12 authors.
Funding
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Abstract
Advanced maternal age increases the risk of pregnancy complications due, in part, to changes in the uterine environment. Here, we show that uterine aging in mice is associated with a progressive increase in transcriptional variation, accompanied by a notable accumulation of activating histone marks at multiple genomic loci. Importantly, the transcriptional signatures of uterine aging differ substantially from senescence markers associated with organismal aging. We demonstrate that maternal age-induced effects largely originate in the epithelial compartment and entail a dramatic up-regulation of the pioneer transcription factor FOXC1, combined with a hyper-enrichment for H3K27ac and H3K4me3 across the locus. FOXC1 over-expression in human endometrial epithelial cells causes profound transcriptomic shifts and increased proliferation, recapitulating the aging phenotype. Using endometrial epithelial organoids of young and aged mice, we find that aging hallmarks including
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