Evidence map›Paper›PMID 37468187›Full record

ArticleJournal of the American College of Cardiology2023

Role of Human Epicardial Adipose Tissue-Derived miR-92a-3p in Myocardial Redox State.

Maria Cristina Carena, Ileana Badi, Murray Polkinghorne, Ioannis Akoumianakis, Costas Psarros, Elizabeth Wahome, Christos P Kotanidis, Nadia Akawi, Alexios S Antonopoulos, Jagat Chauhan and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of the American College of Cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 3 institutions in 2 countries.

Maria Cristina CarenaCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Ileana BadiCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Murray PolkinghorneCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Ioannis AkoumianakisCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Costas PsarrosCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Elizabeth WahomeCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Christos P KotanidisCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Nadia AkawiCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom; Department of Genetics and Genomics, College of Medicine and Health Sciences, United Arab Emirates University, Al-Ain, United Arab Emirates.
Alexios S AntonopoulosCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Jagat ChauhanCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Rana SayeedCardiothoracic Surgery Department, Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom.
George KrasopoulosCardiothoracic Surgery Department, Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom.
Vivek SrivastavaCardiothoracic Surgery Department, Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom.
Shakil FaridCardiothoracic Surgery Department, Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom.
Nicholas WalcotCardiothoracic Surgery Department, Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom.
Gillian DouglasCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Keith M ChannonCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom; Acute Multidisciplinary Imaging and Interventional Centre, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Barbara CasadeiCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Charalambos AntoniadesCardiovascular Medicine Division, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom; Acute Multidisciplinary Imaging and Interventional Centre, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom. Electronic address: antoniad@well.ox.ac.uk.
University of Oxford · GBOxford University Hospitals NHS Trust · GBUnited Arab Emirates University · AE

Funding

British Heart Foundation CH/12/3/29609British Heart Foundation CH/16/1/32013British Heart Foundation CH/F/21/90009British Heart Foundation FS/16/15/32047British Heart Foundation RE/18/3/34214British Heart Foundation RG/16/12/32451British Heart Foundation RG/17/10/32859British Heart Foundation RG/F/21/110040British Heart Foundation RG/F/22/110085British Heart Foundation TG/19/2/34831Department of Health
6 · The paper itself

Abstract

backgroundVisceral obesity is directly linked to increased cardiovascular risk, including heart failure.

objectivesThis study explored the ability of human epicardial adipose tissue (EAT)-derived microRNAs (miRNAs) to regulate the myocardial redox state and clinical outcomes.

methodsThis study screened for miRNAs expressed and released from human EAT and tested for correlations with the redox state in the adjacent myocardium in paired EAT/atrial biopsy specimens from patients undergoing cardiac surgery. Three miRNAs were then tested for causality in an in vitro model of cardiomyocytes. At a clinical level, causality/directionality were tested using genome-wide association screening, and the underlying mechanisms were explored using human biopsy specimens, as well as overexpression of the candidate miRNAs and their targets in vitro and in vivo using a transgenic mouse model. The final prognostic value of the discovered targets was tested in patients undergoing cardiac surgery, followed up for a median of 8 years.

resultsEAT miR-92a-3p was related to lower oxidative stress in human myocardium, a finding confirmed by using genetic regulators of miR-92a-3p in the human heart and EAT. miR-92a-3p reduced nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase-derived superoxide (O

conclusionsEAT-derived miRNAs exert paracrine effects on the human heart. Indeed miR-92a-3p suppresses the wingless-type MMTV integration site family, member 5a/Rac1/NADPH oxidase axis and improves the myocardial redox state. EAT-derived miR-92a-3p is related to improved clinical outcomes and is a rational therapeutic target for the prevention and treatment of obesity-related heart disease.

Indexed as

Genome-Wide Association StudyMicroRNAsAdipose TissueAnimalsHumansMiceMice, TransgenicMyocardiumOxidation-ReductionMicroRNAsepicardial adipose tissuemicroRNAsmyocardial NADPH oxidase activitymyocardial oxidative stressWnt5a signaling

Identifiers

PMID37468187
PMCPMC10368522
OpenAlexW4384500735

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.