Evidence map›Paper›PMID 26146529›Full record

ReviewOxidative medicine and cellular longevity2015

Role of Oxidative Stress in Thyroid Hormone-Induced Cardiomyocyte Hypertrophy and Associated Cardiac Dysfunction: An Undisclosed Story.

Mohammad T Elnakish, Amany A E Ahmed, Peter J Mohler, Paul M L Janssen

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Sage (Anatomy & cell biology · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Functional State of Rat Heart Mitochondria in Experimental Hyperthyroidism.International journal of molecular sciences · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Deficiency of type 2 iodothyronine deiodinase reduces necroptosis activity and oxidative stress responses in retinas of Leber congenital amaurosis model mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Review
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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 3 institutions in 2 countries.

Mohammad T ElnakishDepartment of Physiology and Cell Biology, College of Medicine, The Ohio State University, Columbus, OH 43210, USA ; Dorothy M. Davis Heart & Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA ; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Helwan University, Cairo, Egypt.
Amany A E AhmedDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Helwan University, Cairo, Egypt.
Peter J MohlerDepartment of Physiology and Cell Biology, College of Medicine, The Ohio State University, Columbus, OH 43210, USA ; Dorothy M. Davis Heart & Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA.
Paul M L JanssenDepartment of Physiology and Cell Biology, College of Medicine, The Ohio State University, Columbus, OH 43210, USA ; Dorothy M. Davis Heart & Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA.
Lung Institute · USHelwan University · EGThe Ohio State University · US

Funding

Ohio State Neuroscience Centr CoreP30NS045758 · NINDS · OHIO STATE UNIVERSITY · PI OBRIETAN, KARL H · 2004 to 2015
$7.7M
NINDS NIH HHS P30 NS045758NINDS NIH HHS P30 NS045758-06
6 · The paper itself

Abstract

Cardiac hypertrophy is the most documented cardiomyopathy following hyperthyroidism in experimental animals. Thyroid hormone-induced cardiac hypertrophy is described as a relative ventricular hypertrophy that encompasses the whole heart and is linked with contractile abnormalities in both right and left ventricles. The increase in oxidative stress that takes place in experimental hyperthyroidism proposes that reactive oxygen species are key players in the cardiomyopathy frequently reported in this endocrine disorder. The goal of this review is to shed light on the effects of thyroid hormones on the development of oxidative stress in the heart along with the subsequent cellular and molecular changes. In particular, we will review the role of thyroid hormone-induced oxidative stress in the development of cardiomyocyte hypertrophy and associated cardiac dysfunction, as well as the potential effectiveness of antioxidant treatments in attenuating these hyperthyroidism-induced abnormalities in experimental animal models.

Indexed as

Oxidative StressAnimalsAntioxidantsCardiomegalyHeart VentriclesHyperthyroidismMyocardiumReactive Oxygen SpeciesThyroid HormonesAntioxidantsReactive Oxygen SpeciesThyroid Hormones

Identifiers

PMID26146529
PMCPMC4471379
OpenAlexW2168869551

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.