Evidence map›Paper›PMID 24304833›Full record

ArticleAmerican journal of physiology. Cell physiology2014

Mitochondrial 8-oxoguanine glycosylase decreases mitochondrial fragmentation and improves mitochondrial function in H9C2 cells under oxidative stress conditions.

Moises Torres-Gonzalez, Thomas Gawlowski, Heidi Kocalis, Brian T Scott, Wolfgang H Dillmann

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. The Scavenging Activity of Coenzyme QInternational journal of molecular sciences · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Journal of experimental pharmacology · 2023
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. OGG1 in the Kidney: Beyond Base Excision Repair.Oxidative medicine and cellular longevity · 2022
    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

5 authors at 1 institution in 1 country.

Moises Torres-GonzalezDepartment of Medicine, University of California, San Diego, La Jolla, California.
Thomas Gawlowski
Heidi Kocalis
Brian T Scott
Wolfgang H Dillmann
University of California, San Diego · US

Funding

Vector Production CoreP01HL066941 · NHLBI · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI ROTH, DAVID M · 2001 to 2017
$34.8M
U of Calif, San Diego Neuroscience Microscopy ImagingP30NS047101 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLEESON, JOSEPH G, ZHENG, BINHAI · 2003 to 2022
$9.0M
DIABETIC CARDIOMYOPATHY AND CALCIUM FLUXR01HL066917 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DILLMANN, WOLFGANG H · 2000 to 2011
$4.8M
EXPERIMENTAL ENDOCRINOLOGY AND METABOLISMT32DK007044 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Amit Majithia · 1986 to 2026
$4.6M
NHLBI NIH HHS 5R01HL066917-12NHLBI NIH HHS P01 HL066941NIDDK NIH HHS 3T32DK007044-31S1NIDDK NIH HHS T32 DK007044NINDS NIH HHS P30 NS047101
6 · The paper itself

Abstract

The mitochondrial DNA base modification 8-hydroxy 2'-deoxyguanine (8-OHdG) is one of the most common DNA lesions induced by reactive oxygen species (ROS) and is considered an index of DNA damage. High levels of mitochondrial 8-OHdG have been correlated with increased mutation, deletion, and loss of mitochondrial (mt) DNA, as well as apoptosis. 8-Oxoguanosine DNA glycosylase-1 (OGG1) recognizes and removes 8-OHdG to prevent further DNA damage. We evaluated the effects of OGG1 on mtDNA damage, mitochondrial function, and apoptotic events induced by oxidative stress using H9C2 cardiac cells treated with menadione and transduced with either Adv-Ogg1 or Adv-Control (empty vector). The levels of mtDNA 8-OHdG and the presence of apurinic/apyrimidinic (AP) sites were decreased by 30% and 35%, respectively, in Adv-Ogg1 transduced cells (P < 0.0001 and P < 0.005, respectively). In addition, the expression of base excision repair (BER) pathway members APE1 and DNA polymerase γ was upregulated by Adv-Ogg1 transduction. Cells overexpressing Ogg1 had increased membrane potential (P < 0.05) and decreased mitochondrial fragmentation (P < 0.005). The mtDNA content was found to be higher in cells with increased OGG1 (P < 0.005). The protein levels of fission and apoptotic factors such as DRP1, FIS1, cytoplasmic cytochrome c, activated caspase-3, and activated caspase-9 were lower in Adv-Ogg1 transduced cells. These observations suggest that Ogg1 overexpression may be an important mechanism to protect cardiac cells against oxidative stress damage.

Indexed as

Oxidative Stress8-Hydroxy-2'-DeoxyguanosineAnimalsApoptosisCardiotonic AgentsCaspase 3Caspase 9Cell LineCell SurvivalCytochromes cDNA-(Apurinic or Apyrimidinic Site) LyaseDNA DamageDNA-Directed DNA PolymeraseDNA GlycosylasesDNA, MitochondrialDNA Polymerase gamma8-Hydroxy-2'-Deoxyguanosine8-oxo-7,8-dihydrodeoxyguanineApex1 protein, ratCardiotonic AgentsCaspase 3Caspase 9Cytochromes cDNA-(Apurinic or Apyrimidinic Site) LyaseDNA-Directed DNA PolymeraseDNA GlycosylasesDNA, MitochondrialDNA Polymerase gammaDnm1l protein, ratDynaminsFis1 protein, ratGuanineMitochondrial ProteinsOgg1 protein, mouseVitamin K 38-oxoguanine glycosylaseapoptosismitochondrial DNA damagemitochondrial functionoxidative stress

Identifiers

PMID24304833
PMCPMC3920001
OpenAlexW2074757084

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.