Evidence map›Paper›PMID 30218079›Full record

ArticleScientific reports2018

Integrative analysis of differentially expressed genes and miRNAs predicts complex T3-mediated protective circuits in a rat model of cardiac ischemia reperfusion.

Francesca Forini, Giuseppina Nicolini, Claudia Kusmic, Romina D'Aurizio, Milena Rizzo, Mario Baumgart, Marco Groth, Stefano Doccini, Giorgio Iervasi, Letizia Pitto

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.8field-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

14 citing papers in PubMed, 24 citations in OpenAlex.

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  5. Triiodothyronine maintains cardiac transverse-tubule structure and function.Journal of molecular and cellular cardiology · 2021
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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

10 authors at 5 institutions in 2 countries.

Francesca ForiniInstitute of Clinical Physiology, CNR, Pisa Italy, via G. Moruzzi 1, 56124, Pisa, Italy. simona@ifc.cnr.it.
Giuseppina NicoliniInstitute of Clinical Physiology, CNR, Pisa Italy, via G. Moruzzi 1, 56124, Pisa, Italy.
Claudia KusmicInstitute of Clinical Physiology, CNR, Pisa Italy, via G. Moruzzi 1, 56124, Pisa, Italy.
Romina D'AurizioLaboratory for Integrative System Medicine (LISM), Institute of Informatics and Telematics (IIT), CNR, via G. Moruzzi 1, 56124, Pisa, Italy.ORCID 0000-0002-1728-6397
Milena RizzoInstitute of Clinical Physiology, CNR, Pisa Italy, via G. Moruzzi 1, 56124, Pisa, Italy.ORCID 0000-0001-5924-8615
Mario BaumgartLeibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.ORCID 0000-0001-8172-1595
Marco GrothLeibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.
Stefano DocciniMolecular Medicine, IRCCS Stella Maris, Pisa, Italy.
Giorgio IervasiInstitute of Clinical Physiology, CNR, Pisa Italy, via G. Moruzzi 1, 56124, Pisa, Italy.
Letizia PittoInstitute of Clinical Physiology, CNR, Pisa Italy, via G. Moruzzi 1, 56124, Pisa, Italy.
Istituto di Fisiologia Clinica · ITLeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEFondazione Stella Maris · ITInstitute of Informatics and Telematics · ITIstituto di Scienza e Tecnologie dell'Informazione "Alessandro Faedo" · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thyroid hormone (T3) dyshomeostasis in the cardiac ischemia-reperfusion (IR) setting negatively impacts on mitochondria function and extracellular matrix remodeling. The modulation of cardiac miRNAs may represent the underlying molecular mechanisms, but a systems biology perspective investigating this critical issue in depth is still lacking. A rat model of myocardial IR, with or without an early short-term T3-replacement, was used to predict putative T3-dependent miRNA-gene interactions targeted to mitochondria quality control and wound healing repair. As evidenced by mRNA and miRNA expression profiling, the T3 supplementation reverted the expression of 87 genes and 11 miRNAs that were dysregulated in the untreated group. In silico crossing and functional analysis of the T3-associated differentially expressed transcripts, identified a signature of interconnected miRNA-gene regulatory circuits that confer resistance to noxious cascades of acute stress. In this network the T3-down-regulated Tp53, Jun and Sp1 transcription factors emerge as critical nodes linking intrinsic cell death and oxidative stress pathways to adverse remodeling cascades. The data presented here provide a novel insight into the molecular basis of T3 cardioprotection in the early post-IR phase and highlight the contribution of a previously unappreciated complex T3-regulatory network that may be helpful in translating T3 replacement into clinical practice.

Indexed as

Gene Expression ProfilingAnimalsComputer SimulationDisease Models, AnimalExtracellular MatrixMaleMicroRNAsMitochondriaMyocardial Reperfusion InjuryRatsRats, WistarRNA, MessengerThyroid HormonesMicroRNAsRNA, MessengerThyroid Hormones

Identifiers

PMID30218079
PMCPMC6138681
OpenAlexW2891468663

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.