Evidence map›Paper›PMID 18773293›Full record

ReviewHeart failure reviews2010

Rebuilding the post-infarcted myocardium by activating 'physiologic' hypertrophic signaling pathways: the thyroid hormone paradigm.

Constantinos Pantos, Iordanis Mourouzis, Dennis V Cokkinos

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. The Potential of Thyroid Hormone Therapy in Severe COVID-19: Rationale and Preliminary Evidence.International journal of environmental research and public health · 2022
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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

3 authors at 2 institutions in 2 countries.

Constantinos PantosDepartment of Pharmacology, University of Athens, School of Medicine, 75 Mikras Asias Avenue, 11527 Goudi, Athens, Greece. cpantos@cc.uoa.gr
Iordanis Mourouzis
Dennis V Cokkinos
National and Kapodistrian University of Athens · GROnassis Cardiac Surgery Center · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Viable myocardium undergoes several changes in the course of cardiac remodeling following myocardial infarction aiming to adapt the heart to the hemodynamic compromise. This response is characterized by reactivation of the fetal transcriptional program and results in cardiac dysfunction. Changes in thyroid hormone (TH)-TH receptors (TRs) axis occur in the course of post-infarction cardiac remodeling and seem to contribute to cardiac fetal phenotype. TH can "rebuild" the post-infarcted heart by preventing the fetal-like pattern of contractile proteins expression, normalizing wall tension, and optimizing cardiac chamber geometry. This effect seems to be attributed to TH pleiotropic cellular actions; TH promotes tissue growth and differentiation and favorably remodels cardiac cell while increases cellular survival upon stress. TH may constitute a new therapeutic option for mending the ischemic myocardium.

Indexed as

Ventricular RemodelingAnimalsContractile ProteinsHumansHypertrophyMyocardial InfarctionMyocardiumReceptors, Thyroid HormoneSignal TransductionThyroid HormonesContractile ProteinsReceptors, Thyroid HormoneThyroid Hormones

Identifiers

PMID18773293
OpenAlexW2034720207

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.