Evidence map›Paper›PMID 23160801›Full record

ArticleMolecular and cellular biochemistry2013

Oxidative stress in coronary artery disease: epigenetic perspective.

Sana Venkata Vijaya Lakshmi, Shaik Mohammad Naushad, Cheruku Apoorva Reddy, Kankanala Saumya, Damera Seshagiri Rao, Srigiridhar Kotamraju, Vijay Kumar Kutala

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Extracellular superoxide dismutase and its role in cancer.Free radical biology & medicine · 2017
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 2 institutions in 1 country.

Sana Venkata Vijaya LakshmiDepartment of Clinical Pharmacology & Therapeutics, Nizam's Institute of Medical Sciences, Panjagutta, Hyderabad, 500082, Andhra Pradesh, India.
Shaik Mohammad Naushad
Cheruku Apoorva Reddy
Kankanala Saumya
Damera Seshagiri Rao
Srigiridhar Kotamraju
Vijay Kumar Kutala
Nizam's Institute of Medical Sciences · INIndian Institute of Chemical Technology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The association between oxidative stress and coronary artery disease (CAD) is well documented. However, the role of epigenetic factors contributing to oxidative stress is relatively unexplored. In this study, we aimed to explore the impact of DNA methylation profile in BCL2/E1B adenovirus interacting protein 3 (BNIP3), extracellular superoxide dismutase (EC-SOD) and glutathione-S-transferase P1 (GSTP1) on the oxidative stress in CAD. Further, the contribution of folate pathway genetic polymorphisms in regulating epigenome was elucidated. The expression of BNIP3, EC-SOD, and GSTP1 were studied by using Maxima@SYBR-green based real-time qPCR approach in peripheral blood samples. Combined bisulfite restriction analysis and methylation-specific PCR were used to study promoter CpG island methylation. Further, the effect of homocysteine on BNIP3 gene expression was studied in human aortic endothelial cells in vitro. CAD cases exhibited upregulation of BNIP3, downregulation of EC-SOD and GSTP1. Hypomethylation of BNIP3 and hypermethylation of EC-SOD were observed in CAD cases. The expression of BNIP3 was positively correlated with homocysteine, MDA, protein carbonyls, and methylene tetrahydrofolate reductase C677T, while showing inverse association with cytosolic serine hydroxymethyl transferase C1420T. The expressions of EC-SOD and GSTP1 showed positive association with thymidylate synthase (TYMS) 2R3R, while inverse association with MDA, protein carbonyls, and methionine synthase reductase (MTRR) A66G. In vitro analysis showed homocysteine-dependent upregulation of BNIP3. The results of this study suggest that the aberrations in one-carbon metabolism appear to induce altered gene expression of EC-SOD, GSTP1, and BNIP3, and thus contribute to the increased oxidative stress and increased susceptibility to CAD.

Indexed as

DNA MethylationEpigenesis, GeneticAdultAgedAged, 80 and overAzacitidineCell LineCoronary Artery DiseaseDecitabineEndothelial CellsFemaleFerredoxin-NADP ReductaseFolic AcidGlutathione S-Transferase piGlycine HydroxymethyltransferaseHomocysteineAzacitidineBNIP3 protein, humanDecitabineFerredoxin-NADP ReductaseFolic AcidGlutathione S-Transferase piGlycine HydroxymethyltransferaseGSTP1 protein, humanHomocysteineHydroxamic AcidsMalondialdehydeMembrane Proteinsmethionine synthase reductaseMethylenetetrahydrofolate Reductase (NADPH2)Proto-Oncogene ProteinsSOD3 protein, humanSuperoxide Dismutasetrichostatin A

Identifiers

PMID23160801
OpenAlexW1998428550

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.