Evidence map›Paper›PMID 23323621›Full record

ReviewCurrent pharmaceutical design2013

Cardiac dysfunction and oxidative stress in the metabolic syndrome: an update on antioxidant therapies.

Olesya Ilkun, Sihem Boudina

Open access · bronzeAbstract readReview
In one paragraph

Review in Current pharmaceutical design, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 134 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Metabolic Syndrome-Driven Changes in Cardiac Lymphatic Endothelium: mRNA Expression and Emerging Questions.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Article
  6. Oxidative Modifications in Cardiac Mitochondrial and CaHandbook of experimental pharmacology · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Energy substrate metabolism and oxidative stress in metabolic cardiomyopathy.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  20. Article

2 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Olesya IlkunDivision of Endocrinology, Metabolism and Diabetes, Program in Human Molecular Biology & Genetics, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA.
Sihem Boudina
Diabetes Australia · AU

Funding

Interdisciplinary Training Program in MetabolismT32DK091317 · NIDDK · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI SCOTT A SUMMERS · 2011 to 2026
$4.8M
University of Utah Biomedical Research Core Center (P30) in Metabolism and CVDP30HL101310 · NHLBI · UNIVERSITY OF UTAH · PI ABEL, E DALE · 2009 to 2010
$839k
NHLBI NIH HHS P30 HL101310NHLBI NIH HHS P30-HL-101310NIDDK NIH HHS T32 DK091317NIDDK NIH HHS T32DK091317
6 · The paper itself

Abstract

The metabolic syndrome (MetS) is a cluster of risk factors including obesity, insulin resistance, dyslipidemia, elevated blood pressure and glucose intolerance. The MetS increases the risk for cardiovascular disease (CVD) and type 2 diabetes. Each component of the MetS causes cardiac dysfunction and their combination carries additional risk. The mechanisms underlying cardiac dysfunction in the MetS are complex and might include lipid accumulation, increased fibrosis and stiffness, altered calcium homeostasis, abnormal autophagy, altered substrate utilization, mitochondrial dysfunction and increased oxidative stress. Mitochondrial and extra-mitochondrial sources of reactive oxygen species (ROS) and reduced antioxidant defense mechanisms characterize the myocardium of humans and animals with the MetS. The mechanisms for increased cardiac oxidative stress in the MetS are not fully understood but include increased fatty acid oxidation, mitochondrial dysfunction and enhanced NADPH oxidase activity. Therapies aimed to reduce oxidative stress and enhance antioxidant defense have been employed to reduce cardiac dysfunction in the MetS in animals. In contrast, large scale clinical trials using antioxidants therapies for the treatment of CVD have been disappointing because of the lack of efficacy and undesired side effects. The focus of this review is to summarize the current knowledge about the mechanisms underlying cardiac dysfunction in the MetS with a special interest in the role of oxidative stress. Finally, we will update the reader on the results obtained with natural antioxidant and mitochondria-targeted antioxidant therapies for the treatment of CVD in the MetS.

Indexed as

AnimalsAntioxidantsCardiomyopathiesDiabetes Mellitus, Type 2Diabetic CardiomyopathiesHeartHumansHypoglycemic AgentsMetabolic SyndromeMyocardiumObesityOxidative StressAntioxidantsHypoglycemic Agents

Identifiers

PMID23323621
PMCPMC3856187
OpenAlexW2011521489

What OpenQuestion holds

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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.