Evidence map›Paper›PMID 28727777›Full record

ArticlePloS one2017

8-oxoguanine DNA glycosylase (OGG1) deficiency elicits coordinated changes in lipid and mitochondrial metabolism in muscle.

Vladimir Vartanian, Jana Tumova, Pawel Dobrzyn, Agnieszka Dobrzyn, Yusaku Nakabeppu, R Stephen Lloyd, Harini Sampath

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Frequencies and spectra of aflatoxin BNAR molecular medicine · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. OGG1 in the Kidney: Beyond Base Excision Repair.Oxidative medicine and cellular longevity · 2022
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
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  18. Review
  19. Article
  20. Review
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

7 authors at 4 institutions in 3 countries.

Vladimir VartanianFrom the Oregon Institute of Occupational Health Sciences, Oregon Health & Science University, Portland, Oregon, United States of America.
Jana TumovaDepartment of Nutritional Sciences, Rutgers University, New Brunswick, New Jersey, United States of America.
Pawel DobrzynNencki Institute of Experimental Biology, Warsaw, Poland.
Agnieszka DobrzynNencki Institute of Experimental Biology, Warsaw, Poland.
Yusaku NakabeppuDivision of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
R Stephen LloydFrom the Oregon Institute of Occupational Health Sciences, Oregon Health & Science University, Portland, Oregon, United States of America.
Harini SampathDepartment of Nutritional Sciences, Rutgers University, New Brunswick, New Jersey, United States of America.ORCID http://orcid.org/0000-0001-7339-7115
Instytut Biologii Doświadczalnej im. Marcelego Nenckiego · PLOregon Health & Science University · USRutgers, The State University of New Jersey · USKyushu University · JP

Funding

DNA Repair Deficiency Associated with Obesity and the Metabolic SyndromeR01DK075974 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI LLOYD, R. STEPHEN · 2009 to 2013
$1.7M
Role of oxidative DNA damage in the onset and progression of metabolic syndromeR00DK100640 · NIDDK · RUTGERS, THE STATE UNIV OF N.J. · PI SAMPATH, HARINI · 2016 to 2018
$888k
Role of oxidative DNA damage in the onset and progression of metabolic syndromeK99DK100640 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI SAMPATH, HARINI · 2014 to 2015
$180k
DNA Repair Deficiency Associated with Obesity and the Meatbolic SyndromeR56DK075974 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI LLOYD, R STEPHEN · 2007 to 2007
$115k
NIDDK NIH HHS K99 DK100640NIDDK NIH HHS R00 DK100640NIDDK NIH HHS R01 DK075974NIDDK NIH HHS R56 DK075974
6 · The paper itself

Abstract

Oxidative stress resulting from endogenous and exogenous sources causes damage to cellular components, including genomic and mitochondrial DNA. Oxidative DNA damage is primarily repaired via the base excision repair pathway that is initiated by DNA glycosylases. 8-oxoguanine DNA glycosylase (OGG1) recognizes and cleaves oxidized and ring-fragmented purines, including 8-oxoguanine, the most commonly formed oxidative DNA lesion. Mice lacking the OGG1 gene product are prone to multiple features of the metabolic syndrome, including high-fat diet-induced obesity, hepatic steatosis, and insulin resistance. Here, we report that OGG1-deficient mice also display skeletal muscle pathologies, including increased muscle lipid deposition and alterations in genes regulating lipid uptake and mitochondrial fission in skeletal muscle. In addition, expression of genes of the TCA cycle and of carbohydrate and lipid metabolism are also significantly altered in muscle of OGG1-deficient mice. These tissue changes are accompanied by marked reductions in markers of muscle function in OGG1-deficient animals, including decreased grip strength and treadmill endurance. Collectively, these data indicate a role for skeletal muscle OGG1 in the maintenance of optimal tissue function.

Indexed as

AdiposityAnimalsDNA DamageDNA GlycosylasesDNA, MitochondrialFatty AcidsGene Expression ProfilingLipid MetabolismMaleMice, Inbred C57BLMitochondriaMitochondrial DynamicsModels, AnimalMuscle, SkeletalMuscle StrengthPhysical EnduranceDNA GlycosylasesDNA, MitochondrialFatty AcidsOgg1 protein, mousePyruvic Acid

Identifiers

PMID28727777
PMCPMC5519207
OpenAlexW2737561488

What OpenQuestion holds

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LicenceCC BY
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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.