Evidence map›Paper›PMID 20100314›Full record

ArticleJournal of cellular and molecular medicine2011

Early long-term L-T3 replacement rescues mitochondria and prevents ischemic cardiac remodelling in rats.

Francesca Forini, Vincenzo Lionetti, Hossein Ardehali, Angela Pucci, Federica Cecchetti, Mohsen Ghanefar, Giuseppina Nicolini, Yoshihiko Ichikawa, Monica Nannipieri, Fabio A Recchia and 1 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

49 citing papers in PubMed, 95 citations in OpenAlex.

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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

11 authors at 6 institutions in 2 countries.

Francesca ForiniInstitute of Clinical Physiology, CNR, Pisa, Italy.
Vincenzo Lionetti
Hossein Ardehali
Angela Pucci
Federica Cecchetti
Mohsen Ghanefar
Giuseppina Nicolini
Yoshihiko Ichikawa
Monica Nannipieri
Fabio A Recchia
Giorgio Iervasi
Istituto di Fisiologia Clinica · ITNorthwestern University · USUniversity of Pisa · ITAzienda Ospedaliera Universitaria Pisana · ITNew York Medical College · USZero to Three · US

Funding

Role of the mitochondrial ATP-binding cassette protein-1 in cellular protectionR01HL087149 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ARDEHALI, HOSSEIN · 2007 to 2011
$2.1M
VEGF receptor-1-mediated protection in dilated cardiomyopathyR01HL108213 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI RECCHIA, FABIO A · 2012 to 2015
$1.6M
Functional Characterization of mABC1 ProteinK08HL079387 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ARDEHALI, HOSSEIN · 2005 to 2009
$629k
NHLBI NIH HHS K08 HL079387NHLBI NIH HHS R01 HL087149NHLBI NIH HHS R01 HL108213
6 · The paper itself

Abstract

3,5,3'-Levo-triiodothyronine (L-T3) is essential for DNA transcription, mitochondrial biogenesis and respiration, but its circulating levels rapidly decrease after myocardial infarction (MI). The main aim of our study was to test whether an early and sustained normalization of L-T3 serum levels after MI exerts myocardial protective effects through a mitochondrial preservation. Seventy-two hours after MI induced by anterior interventricular artery ligation, rats were infused with synthetic L-T3 (1.2 μg/kg/day) or saline over 4 weeks. Compared to saline, L-T3 infusion restored FT3 serum levels at euthyroid state (3.0 ± 0.2 versus 4.2 ± 0.3 pg/ml), improved left ventricular (LV) ejection fraction (39.5 ± 2.5 versus 65.5 ± 6.9%), preserved LV end-systolic wall thickening in the peri-infarct zone (6.34 ± 3.1 versus 33.7 ± 6.21%) and reduced LV infarct-scar size by approximately 50% (all P < 0.05). Moreover, L-T3 significantly increased angiogenesis and cell survival and enhanced the expression of nuclear-encoded transcription factors involved in these processes. Finally, L-T3 significantly increased the expression of factors involved in mitochondrial DNA transcription and biogenesis, such as hypoxic inducible factor-1α, mitochondrial transcription factor A and peroxisome proliferator activated receptor γ coactivator-1α, in the LV peri-infarct zone. To further explore mechanisms of L-T3 protective effects, we exposed isolated neonatal cardiomyocytes to H(2)O(2) and found that L-T3 rescued mitochondrial biogenesis and function and protected against cell death via a mitoKATP dependent pathway. Early and sustained physiological restoration of circulating L-T3 levels after MI halves infarct scar size and prevents the progression towards heart failure. This beneficial effect is likely due to enhanced capillary formation and mitochondrial protection.

Indexed as

Hormone Replacement TherapyAnimalsApoptosisBlotting, WesternCapillariesCells, CulturedHemodynamicsHydrogen PeroxideHypoxia-Inducible Factor 1, alpha SubunitInfusions, SubcutaneousMaleMitochondriaMyocardial InfarctionMyocytes, CardiacOxidantsRandom AllocationHif1a protein, ratHydrogen PeroxideHypoxia-Inducible Factor 1, alpha SubunitOxidantsThyroxineTriiodothyronine

Identifiers

PMID20100314
PMCPMC3922373
OpenAlexW2013644808

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.