Evidence map›Paper›PMID 22302830›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2012

Nutrient deprivation regulates DNA damage repair in cardiomyocytes via loss of the base-excision repair enzyme OGG1.

Lee Siggens, Nichola Figg, Martin Bennett, Roger Foo

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.5field-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

39 citing papers in PubMed, 60 citations in OpenAlex.

  1. DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  2. Cardiomyopathies and a brief insight into DOX-induced cardiomyopathy.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. OGG1 in the Kidney: Beyond Base Excision Repair.Oxidative medicine and cellular longevity · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Cardiomyocyte Proliferative Capacity Is Restricted in Mice WithFrontiers in cardiovascular medicine · 2021
    Article
  17. Crosstalk between autophagy and DNA repair systems.Turkish journal of biology = Turk biyoloji dergisi · 2021
    Article
  18. How Far Are We from Prescribing Fasting as Anticancer Medicine?International journal of molecular sciences · 2020
    Review
  19. Review
  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

4 authors at 2 institutions in 1 country.

Lee SiggensDivision of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Centre of Clinical Investigation Building, Level 6, Addenbrooke's Hospital, Cambridge, CB2 0QQ, UK.
Nichola Figg
Martin Bennett
Roger Foo
Addenbrooke's Hospital · GBUniversity of Cambridge · GB

Funding

British Heart Foundation RG/08/009/25841Medical Research Council G0800784Medical Research Council G1000847Wellcome Trust 086797
6 · The paper itself

Abstract

Oxidative stress contributes to the pathogenesis of many diseases, including heart failure, but the role and regulation of oxidative DNA damage in many cases have not been studied. Here, we set out to examine how oxidative DNA damage is regulated in cardiomyocytes. Compared to normal healthy controls, human hearts in end-stage cardiomyopathy (EsCM) showed a high degree of DNA damage by histological evidence of damage markers, including 8-oxoG and γH2AX (8-oxoG: 4.7±0.88 vs. 99.9±0.11%; γH2AX: 2.1±0.33 vs. 85.0±13.8%; P<0.01) This raised the possibility that defective DNA repair may be partly responsible. Indeed, nutrient deprivation led to impaired base-excision repair (BER) in cardiomyocytes in vitro, accompanied by loss of the BER enzyme OGG1, while BER activity was rescued by recombinant OGG1 (control vs. nutrient deprived vs. nutrient deprived+OGG1; 100±2.96 vs. 68.2±7.53 vs. 94.0±0.72%; ANOVA, P<0.01). Hearts from humans with EsCM and two murine models of myocardial stress also showed a loss of OGG1 protein. OGG1 loss was inhibited by the autophagy inhibitor bafilomycin and in autophagy-deficient Atg5(-/-) mouse embryonic fibroblasts. However, pharmacological activation of autophagy, itself, did not induce OGG1 loss, suggesting that autophagy is necessary but not sufficient for OGG1 turnover, and OGG1 loss requires concurrent nutrient deprivation. Finally, we found that the role of autophagy in nutrient starvation is complex, since it balanced the positive effects of ROS inhibition against the negative effect of OGG1 loss. Therefore, we have identified a central role for OGG1 in regulating DNA repair in cardiomyopathy. The manipulation of OGG1 may be used in future studies to examine the direct contribution of oxidative DNA damage to the progression of heart failure.

Indexed as

DNA DamageDNA RepairAnimalsBase SequenceDNA GlycosylasesDNA PrimersHumansImmunohistochemistryMiceMyocardiumDNA GlycosylasesDNA Primersoxoguanine glycosylase 1, human

Identifiers

PMID22302830
PMCPMC3630495
OpenAlexW2114331892

What OpenQuestion holds

Textmetadata
LicenceTDM
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.