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dc.contributor.authorLock, Mitchell C
dc.contributor.authorBotting, Kimberley J
dc.contributor.authorTellam, Ross L
dc.contributor.authorBrooks, Doug
dc.contributor.authorMorrison, Janna L
dc.date.accessioned2018-04-10T17:05:24Z
dc.date.available2018-04-10T17:05:24Z
dc.date.issued2017-12-06
dc.identifier.issn1661-6596
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/274749
dc.description.abstractPlacental insufficiency, high altitude pregnancies, maternal obesity/diabetes, maternal undernutrition and stress can result in a poor setting for growth of the developing fetus. These adverse intrauterine environments result in physiological changes to the developing heart that impact how the heart will function in postnatal life. The intrauterine environment plays a key role in the complex interplay between genes and the epigenetic mechanisms that regulate their expression. In this review we describe how an adverse intrauterine environment can influence the expression of miRNAs (a sub-set of non-coding RNAs) and how these changes may impact heart development. Potential consequences of altered miRNA expression in the fetal heart include; Hypoxia inducible factor (HIF) activation, dysregulation of angiogenesis, mitochondrial abnormalities and altered glucose and fatty acid transport/metabolism. It is important to understand how miRNAs are altered in these adverse environments to identify key pathways that can be targeted using miRNA mimics or inhibitors to condition an improved developmental response.
dc.format.mediumElectronic
dc.languageeng
dc.language.isoen
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectFetal Heart
dc.subjectAnimals
dc.subjectHumans
dc.subjectMicroRNAs
dc.subjectEnvironment
dc.subjectAcclimatization
dc.subjectEpigenesis, Genetic
dc.subjectStress, Physiological
dc.titleAdverse Intrauterine Environment and Cardiac miRNA Expression.
dc.typeArticle
prism.issueIdentifier12
prism.publicationDate2017
prism.publicationNameInt J Mol Sci
prism.volume18
dc.identifier.doi10.17863/CAM.21877
dcterms.dateAccepted2017-11-28
rioxxterms.versionofrecord10.3390/ijms18122628
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2017-12-06
dc.contributor.orcidLock, Mitchell C [0000-0002-3594-1455]
dc.contributor.orcidTellam, Ross L [0000-0003-2353-1640]
dc.contributor.orcidMorrison, Janna L [0000-0002-8602-8519]
dc.identifier.eissn1422-0067
rioxxterms.typeJournal Article/Review
cam.issuedOnline2017-12-06


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International