Evidence map›Paper›PMID 29733330›Full record

ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2019

Benefits of Caloric Restriction in Longevity and Chemical-Induced Tumorigenesis Are Transmitted Independent of NQO1.

Alberto Diaz-Ruiz, Andrea Di Francesco, Bethany A Carboneau, Sophia R Levan, Kevin J Pearson, Nathan L Price, Theresa M Ward, Michel Bernier, Rafael de Cabo, Evi M Mercken

Open access · hybridAbstract read
In one paragraph

Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  6. NADH/NADBiomolecules · 2021
    Review
  7. Review
  8. NADNature reviews. Molecular cell biology · 2021
    Review
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  11. Article
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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

10 authors at 4 institutions in 2 countries.

Alberto Diaz-RuizTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland.
Andrea Di FrancescoTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland.
Bethany A CarboneauTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland.
Sophia R LevanTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland.
Kevin J PearsonDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington.
Nathan L PriceVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT.
Theresa M WardTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland.
Michel BernierTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland.
Rafael de CaboTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland.
Evi M MerckenTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland.
National Institutes of Health · USMadrid Institute for Advanced Studies · ESUniversity of Kentucky · USYale University · US

Funding

Calorie restriction and agingZIAAG000368 · NIA · NATIONAL INSTITUTE ON AGING · PI DE CABO, RAFAEL · 2009 to 2025
$6.9M
Aging and CR effects on the Plasma Membrane Redox SystemZIAAG000362 · NIA · NATIONAL INSTITUTE ON AGING · PI DE CABO, RAFAEL · 2009 to 2025
$5.0M
6 · The paper itself

Abstract

Caloric restriction (CR) is the most potent nonpharmacological intervention known to both protect against carcinogenesis and delay aging in laboratory animals. There is a growing number of anticarcinogens and CR mimetics that activate NAD(P)H:quinone oxidoreductase 1 (NQO1). We have previously shown that NQO1, an antioxidant enzyme that acts as an energy sensor through modulation of intracellular redox and metabolic state, is upregulated by CR. Here, we used NQO1-knockout (KO) mice to investigate the role of NQO1 in both the aging process and tumor susceptibility, specifically in the context of CR. We found that NQO1 is not essential for the beneficial effects of CR on glucose homeostasis, physical performance, metabolic flexibility, life-span extension, and (unlike our previously observation with Nrf2) chemical-induced tumorigenesis.

Indexed as

Body CompositionLongevityOxidative StressAnimalsBiomarkers, TumorCaloric RestrictionCarcinogenesisImmunoblottingMaleMiceMice, Inbred C57BLMice, KnockoutNAD(P)H Dehydrogenase (Quinone)Neoplasms, ExperimentalBiomarkers, TumorNAD(P)H Dehydrogenase (Quinone)Nqo1 protein, mouse

Identifiers

PMID29733330
PMCPMC6599277
OpenAlexW2802114599

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.