ArticleAging2016
Early age decline in DNA repair capacity in the liver: in depth profile of differential gene expression.
Article in Aging, 2016. 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 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
13 citing papers in PubMed, 22 citations in OpenAlex.
- Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025Review
- Senataxin Attenuates DNA Damage Response Activation and Suppresses Senescence.Antioxidants (Basel, Switzerland) · 2024Article
- Genomic Instability and Epigenetic Changes during Aging.International journal of molecular sciences · 2023Review
- Magnesium and Liver Metabolism Through the Lifespan.Advances in nutrition (Bethesda, Md.) · 2023Review
- The DNA damage response pathway regulates the expression of the immune checkpoint CD47.Communications biology · 2023Article
- Intestinal microbiota: a new perspective on delaying aging?Frontiers in microbiology · 2023Review
- Bladder cancer, inflammageing and microbiomes.Nature reviews. Urology · 2022Review
- Review
- DNA damage alters EGFR signaling and reprograms cellular response via Mre-11.Scientific reports · 2022Article
- Persistent hepatocyte apoptosis promotes tumorigenesis from diethylnitrosamine-transformed hepatocytes through increased oxidative stress, independent of compensatory liver regeneration.Scientific reports · 2021Article
- Endocrine disruptor exposure during development increases incidence of uterine fibroids by altering DNA repair in myometrial stem cells.Biology of reproduction · 2018Article
- Early-onset liver cancer in South America associates with low hepatitis B virus DNA burden.Scientific reports · 2018Article
- Deficiency in DNA damage response of enterocytes accelerates intestinal stem cell aging inAging · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is associated with progressive decline in cell function and with increased damage to macromolecular components. DNA damage, in the form of double-strand breaks (DSBs), increases with age and in turn, contributes to the aging process and age-related diseases. DNA strand breaks triggers a set of highly orchestrated signaling events known as the DNA damage response (DDR), which coordinates DNA repair. However, whether the accumulation of DNA damage with age is a result of decreased repair capacity, remains to be determined. In our study we showed that with age there is a decline in the resolution of foci containing γH2AX and pKAP-1 in diethylnitrosamine (DEN)-treated mouse livers, already evident at a remarkably early age of 6-months. Considerable age-dependent differences in global gene expression profiles in mice livers after exposure to DEN, further affirmed these age related differences in the response to DNA damage. Functional analysis identified p53 as the most overrepresented pathway that is specifically enhanced and prolonged in 6-month-old mice. Collectively, our results demonstrated an early decline in DNA damage repair that precedes 'old age', suggesting this may be a driving force contributing to the aging process rather than a phenotypic consequence of old age.
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What OpenQuestion holds
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.