Evidence map›Paper›PMID 24693334›Full record

ArticleOxidative medicine and cellular longevity2014

Enhancement of cellular antioxidant-defence preserves diastolic dysfunction via regulation of both diastolic Zn2+ and Ca2+ and prevention of RyR2-leak in hyperglycemic cardiomyocytes.

Erkan Tuncay, Esma N Okatan, Aysegul Toy, Belma Turan

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
  2. ZnT6-mediated ZnMolecular and cellular biochemistry · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. CaPflugers Archiv : European journal of physiology · 2022
    Review
  8. Review
  9. The role of labile ZnMolecular and cellular biochemistry · 2021
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Increased free ZnJournal of cellular and molecular medicine · 2018
    Article
  15. Article
  16. Review
  17. Impact of Labile Zinc on Heart Function: From Physiology to Pathophysiology.International journal of molecular sciences · 2017
    Review
  18. Dysregulated ZnThe Journal of biological chemistry · 2017
    Article
  19. Article
  20. The Critical Roles of Zinc: Beyond Impact on Myocardial Signaling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015
    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 1 institution in 1 country.

Erkan TuncayDepartment of Biophysics, Faculty of Medicine, Ankara University, Ankara 06100, Turkey.
Esma N OkatanDepartment of Biophysics, Faculty of Medicine, Ankara University, Ankara 06100, Turkey.
Aysegul ToyDepartment of Biophysics, Faculty of Medicine, Ankara University, Ankara 06100, Turkey.
Belma TuranDepartment of Biophysics, Faculty of Medicine, Ankara University, Ankara 06100, Turkey.
Ankara University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We examined whether cellular antioxidant-defence enhancement preserves diastolic dysfunction via regulation of both diastolic intracellular free Zn(2+) and Ca(2+) levels ([Zn(2+)]i and [Ca(2+)]i) levels N-acetyl cysteine (NAC) treatment (4 weeks) of diabetic rats preserved altered cellular redox state and also prevented diabetes-induced tissue damage and diastolic dysfunction with marked normalizations in the resting [Zn(2+)]i and [Ca(2+)]i. The kinetic parameters of transient changes in Zn(2+) and Ca(2+) under electrical stimulation and the spatiotemporal properties of Zn(2+) and Ca(2+) sparks in resting cells are found to be normal in the treated diabetic group. Biochemical analysis demonstrated that the NAC treatment also antagonized hyperphosphorylation of cardiac ryanodine receptors (RyR2) and significantly restored depleted protein levels of both RyR2 and calstabin2. Incubation of cardiomyocytes with 10 µM ZnCl2 exerted hyperphosphorylation in RyR2 as well as higher phosphorphorylations in both PKA and CaMKII in a concentration-dependent manner, similar to hyperglycemia. Our present data also showed that a subcellular oxidative stress marker, NF-κB, can be activated if the cells are exposed directly to Zn(2+). We thus for the first time report that an enhancement of antioxidant defence in diabetics via directly targeting heart seems to prevent diastolic dysfunction due to modulation of RyR2 macromolecular-complex thereby leading to normalized [Ca(2+)]i and [Zn(2+)]i in cardiomyocytes.

Indexed as

DiastoleAcetylcysteineAnimalsAntioxidantsBlood GlucoseBody WeightCalciumDiabetes Mellitus, ExperimentalHeart VentriclesHyperglycemiaIntracellular SpaceIn Vitro TechniquesMaleMyocardiumMyocytes, CardiacNF-kappa BAcetylcysteineAntioxidantsBlood GlucoseCalciumNF-kappa BRyanodine Receptor Calcium Release ChannelTacrolimus Binding ProteinsZinc

Identifiers

PMID24693334
PMCPMC3945998
OpenAlexW1508543190

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.