Evidence map›Paper›PMID 25645467›Full record

ReviewAging cell2015

Aging and radiation: bad companions.

Laia Hernández, Mariona Terradas, Jordi Camps, Marta Martín, Laura Tusell, Anna Genescà

Open access · goldAbstract readReview
In one paragraph

Review in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.8field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 92 citations in OpenAlex.

  1. Terpenoids as modulators of autophagy-senescence crosstalk in lung cancer.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
  2. Impact of CaInternational journal of molecular sciences · 2026
    Review
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  15. Aging by autodigestion.PloS one · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Laia HernándezDepartment of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, 08193, Bellaterra, Spain.
Mariona Terradas
Jordi Camps
Marta Martín
Laura Tusell
Anna Genescà
Universitat Autònoma de Barcelona · ESCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging involves a deterioration of cell functions and changes that may predispose the cell to undergo an oncogenic transformation. The carcinogenic risks following radiation exposure rise with age among adults. Increasing inflammatory response, loss of oxidant/antioxidant equilibrium, ongoing telomere attrition, decline in the DNA damage response efficiency, and deleterious nuclear organization are age-related cellular changes that trigger a serious threat to genomic integrity. In this review, we discuss the mechanistic interplay between all these factors, providing an integrated view of how they contribute to the observed age-related increase in radiation sensitivity. As life expectancy increases and so it does the medical intervention, it is important to highlight the benefits of radiation protection in the elderly. Thus, a deep understanding of the mechanistic processes confining the threat of aging-related radiosensitivity is currently of foremost relevance.

Indexed as

Age FactorsAgingAnimalsDNA DamageHumansRadiation Injurieschromatin organizationDNA repairnuclear envelopeoxidative stressradiosensitivityreplicative senescence

Identifiers

PMID25645467
PMCPMC4364827
OpenAlexW2043527236

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.