ArticleAging cell2025
Aging Increases Short, Inverted Repeat-Mediated Genomic Instability In Vivo.
Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Non-B DNA structures and their contributions to genetic diversity, aging, and disease.Nucleic acids research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Genomic instability is a hallmark of aging and cancer. A key contributor to genomic instability includes alternative DNA structures, such as cruciform-forming inverted repeats (IRs). Short IRs (< 100 bps) are abundant in the human genome, mutagenic, and enriched at mutation hotspots in human cancer genomes. Using an innovative mutation-reporter mouse model, we showed that short IRs are mutagenic in vivo. Further, we found that aging exacerbates IR-induced genomic instability, as evidenced by increased mutation frequencies and altered spectra in the spleen and brain of mice harboring either a short IR or control B-DNA sequence at 2 and 24 months of age. These findings establish a link between aging and enhanced mutagenesis at short IRs, providing a unique in vivo platform to investigate age-related mechanisms of DNA structure-mediated genomic instability.
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Registered trials
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