Evidence map›Paper›PMID 23532677›Full record

ArticleMolecular and cellular biochemistry2013

Inhibition of thyroid hormone receptor α1 impairs post-ischemic cardiac performance after myocardial infarction in mice.

Iordanis Mourouzis, Erietta Kostakou, Georgios Galanopoulos, Polixeni Mantzouratou, Constantinos Pantos

Abstract read
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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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. The abnormal thyroxine signals triggers podocyte apoptosis in DN mice.In vitro cellular & developmental biology. Animal · 2026
    Article
  3. Article
  4. Review
  5. Knockout of ACE-N facilitates improved cardiac function after myocardial infarction.Journal of molecular and cellular cardiology plus · 2023
    Article
  6. Developmental changes of the fetal and neonatal thyroid gland and functional consequences on the cardiovascular system.Journal of perinatology : official journal of the California Perinatal Association · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
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  16. Article
  17. Observational
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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

5 authors at 1 institution in 1 country.

Iordanis MourouzisDepartment of Pharmacology, University of Athens, Athens, Greece.
Erietta Kostakou
Georgios Galanopoulos
Polixeni Mantzouratou
Constantinos Pantos
National and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thyroid hormone receptor α1 (TRα1) is shown to be critical for the maturation of cardiomyocytes and for the cellular response to stress. TRα1 is altered during post ischemic cardiac remodeling but the physiological significance of this response is not fully understood. Thus, the present study explored the potential consequences of selective pharmacological inhibition of TRα1 on the mechanical performance of the post-infarcted heart. Acute myocardial infarction was induced in mice (AMI), while sham operated animals served as controls (SHAM). A group of mice was treated with debutyl-dronedarone (DBD), a selective TRα1 inhibitor (AMI-DBD). AMI resulted in low T3 levels in plasma and in down-regulation of TRα1 and TRβ1 expression. Left ventricular ejection fraction (LVEF%) was significantly reduced in AMI [33 (SEM 2.1) vs 79(2.5) in SHAM, p < 0.05] and was further declined in AMI-DBD [22(1.1) vs 33(2.1), respectively, p < 0.05]. Cardiac mass was increased in AMI but not in AMI-DBD hearts, resulting in significant increase in wall tension index. This increase in wall stress was accompanied by marked activation of p38 MAPK, a kinase that is sensitive to mechanical stretch and exerts negative inotropic effect. Furthermore, AMI resulted in β-myosin heavy chain overexpression and reduction in the ratio of SR(Ca)ATPase to phospholamban (PLB). The latter further declined in AMI-DBD mainly due to increased expression of PLB. AMI induces downregulation of thyroid hormone signaling and pharmacological inhibition of TRα1 further depresses post-ischemic cardiac function. p38 MAPK and PLB may, at least in part, be involved in this response.

Indexed as

AmiodaroneAnimalsCalcium-Binding ProteinsDronedaroneHypertrophy, Left VentricularMaleMiceMice, Inbred C57BLMyocardial InfarctionMyocardial IschemiaMyosinsOrgan SizePhospholambanProtein IsoformsSarcoplasmic Reticulum Calcium-Transporting ATPasesSignal TransductionAmiodaroneCalcium-Binding Proteinsdebutyl-dronedaroneDronedaroneMyosinsPhospholambanProtein IsoformsSarcoplasmic Reticulum Calcium-Transporting ATPasesThyroid Hormone Receptors alphaThyroid Hormones

Identifiers

PMID23532677
OpenAlexW2008168778

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.