Evidence map›Paper›PMID 37073128›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2023

MicroRNA-216a is essential for cardiac angiogenesis.

Rio P Juni, Jordy M M Kocken, Ricardo C Abreu, Lara Ottaviani, Tim Davalan, Burcu Duygu, Ella M Poels, Aliaksei Vasilevich, Jana C Hegenbarth, Mahesh Appari and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

7 citing papers in PubMed, 12 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

18 authors at 6 institutions in 5 countries.

Rio P JuniCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands; Department of Physiology, Amsterdam University Medical Centers, De Boelelaan 1117, 1081 HV Amsterdam, the Netherlands.
Jordy M M KockenCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands.
Ricardo C AbreuCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands; Biomaterials and Stem Cell Based Therapeutics Group, CNC-Center for Neuroscience and Cell Biology, CIBB-Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, UC, Biotech Parque Tecnológico de Cantanhede, 3060-197 Coimbra, Portugal.
Lara OttavianiCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands.
Tim DavalanCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands.
Burcu DuyguCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands.
Ella M PoelsCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands.
Aliaksei VasilevichDepartment of Biomedical Engineering and Institute for Complex Molecular Systems, University of Eindhoven, Eindhoven, the Netherlands.
Jana C HegenbarthCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands.
Mahesh AppariDivision of Cardiovascular Medicine, British Heart Foundation Centre of Research Excellence, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 9DU United Kingdom.
Nicole BitschCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands.
Serve OlieslagersCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands.
Dorien M SchrijversLaboratory of Physiopharmacology, University of Antwerp, 2610 Wilrijk, Belgium.
Monika StollDepartment of Genetic Epidemiology, Institute of Human Genetics, University of Münster, 48149 Münster, Germany; Department of Biochemistry, CARIM School for Cardiovascular Diseases, Maastricht University, 6229 ER Maastricht, the Netherlands.
Joerg HeinekeDepartment of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany; DZHK, Partner Site Heidelberg/Mannheim, 69120 Heidelberg, Germany.
Jan de BoerDepartment of Biomedical Engineering and Institute for Complex Molecular Systems, University of Eindhoven, Eindhoven, the Netherlands.
Leon J de WindtCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands.
Paula A da Costa MartinsCARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, the Netherlands; Department of Surgery and Physiology, Faculty of Medicine of the University of Porto, 4200-319 Porto, Portugal. Electronic address: p.dacostamartins@maastrichtuniversity.nl.
Maastricht University · NLEindhoven University of Technology · NLBritish Heart Foundation · GBHeidelberg University · DEUniversity of Antwerp · BEUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While it is experimentally supported that impaired myocardial vascularization contributes to a mismatch between myocardial oxygen demand and supply, a mechanistic basis for disruption of coordinated tissue growth and angiogenesis in heart failure remains poorly understood. Silencing strategies that impair microRNA biogenesis have firmly implicated microRNAs in the regulation of angiogenesis, and individual microRNAs prove to be crucial in developmental or tumor angiogenesis. A high-throughput functional screening for the analysis of a whole-genome microRNA silencing library with regard to their phenotypic effect on endothelial cell proliferation as a key parameter, revealed several anti- and pro-proliferative microRNAs. Among those was miR-216a, a pro-angiogenic microRNA which is enriched in cardiac microvascular endothelial cells and reduced in expression under cardiac stress conditions. miR-216a null mice display dramatic cardiac phenotypes related to impaired myocardial vascularization and unbalanced autophagy and inflammation, supporting a model where microRNA regulation of microvascularization impacts the cardiac response to stress.

Indexed as

Heart FailureMicroRNAsAnimalsEndothelial CellsMiceMyocardiumNeovascularization, PathologicNeovascularization, PhysiologicMicroRNAsMIRN216 microRNA, mouseangiogenesisautophagycardiac remodelingendothelial cellsheart failuremicroRNAs

Identifiers

PMID37073128
PMCPMC10277893
OpenAlexW4366085222

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.