Evidence map›Paper›PMID 19228786›Full record

ReviewThe journals of gerontology. Series A, Biological sciences and medical sciences2009

Does damage to DNA and other macromolecules play a role in aging? If so, how?

Judith Campisi, Jan Vijg

Open access · bronzeAbstract readReview
In one paragraph

Review in The journals of gerontology. Series A, Biological sciences and medical sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.0field-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

57 citing papers in PubMed, 100 citations in OpenAlex.

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  10. Current status and challenges of breast cancer prevention~DNA methylation would lead to groundbreaking progress in breast cancer prevention~.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023
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  17. The Aging Stress Response and Its Implication for AMD Pathogenesis.International journal of molecular sciences · 2020
    Review
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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

2 authors at 2 institutions in 1 country.

Judith CampisiLawrence Berkeley National Laboratory, Life Sciences Division, 1 Cyclotron Road, Berkeley, CA 94720, USA. jcampisi@buckinstitute.org
Jan Vijg
Albert Einstein College of Medicine · USBuck Institute for Research on Aging · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the most pervasive ideas regarding the causes of aging is that longevity is constrained in large measure by damage to macromolecules. An increasing body of cellular and molecular data, generated over the past decade or so, has generally supported this "damage accumulation" hypothesis of aging. There remain unanswered questions regarding which types of damage are most important for driving aging. In addition, there have been recent challenges to the damage accumulation hypothesis and a new emphasis on the importance of cellular responses and the sequelae to damage, rather damage per se. New tools and approaches are on the horizon and will need to be developed and implemented before we can fully understand whether and to what extent macromolecular damage drives aging phenotypes.

Indexed as

AgedAged, 80 and overAgingAnimalsApoptosisCellular SenescenceDNA DamageDrosophilaHumansMacromolecular SubstancesMiceMice, TransgenicModels, AnimalOxidative StressRatsReactive Oxygen SpeciesMacromolecular SubstancesReactive Oxygen Species

Identifiers

PMID19228786
PMCPMC2655027
OpenAlexW2167253194

What OpenQuestion holds

Textmetadata
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.