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dc.contributor.authorQuttainah, Mohammed
dc.contributor.authorRaveendran, Vineesh Vimala
dc.contributor.authorSaleh, Soad
dc.contributor.authorParhar, Ranjit
dc.contributor.authorAljoufan, Mansour
dc.contributor.authorMoorjani, Narain
dc.contributor.authorAl-Halees, Zohair Y
dc.contributor.authorAlShahid, Maie
dc.contributor.authorCollison, Kate S
dc.contributor.authorWestaby, Stephen
dc.contributor.authorAl-Mohanna, Futwan
dc.date.accessioned2022-06-29T19:48:48Z
dc.date.available2022-06-29T19:48:48Z
dc.date.issued2022-05-23
dc.identifier.issn2218-273X
dc.identifier.other35625658
dc.identifier.otherPMC9138767
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/338572
dc.description.abstractCurrent management of heart failure (HF) is centred on modulating the progression of symptoms and severity of left ventricular dysfunction. However, specific understandings of genetic and molecular targets are needed for more precise treatments. To attain a clearer picture of this, we studied transcriptome changes in a chronic progressive HF model. Fifteen sheep (Ovis aries) underwent supracoronary aortic banding using an inflatable cuff. Controlled and progressive induction of pressure overload in the LV was monitored by echocardiography. Endomyocardial biopsies were collected throughout the development of LV failure (LVF) and during the stage of recovery. RNA-seq data were analysed using the PANTHER database, Metascape, and DisGeNET to annotate the gene expression for functional ontologies. Echocardiography revealed distinct clinical differences between the progressive stages of hypertrophy, dilatation, and failure. A unique set of transcript expressions in each stage was identified, despite an overlap of gene expression. The removal of pressure overload allowed the LV to recover functionally. Compared to the control stage, there were a total of 256 genes significantly changed in their expression in failure, 210 genes in hypertrophy, and 73 genes in dilatation. Gene expression in the recovery stage was comparable with the control stage with a well-noted improvement in LV function. RNA-seq revealed the expression of genes in each stage that are not reported in cardiovascular pathology. We identified genes that may be potentially involved in the aetiology of progressive stages of HF, and that may provide future targets for its management.
dc.languageeng
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceessn: 2218-273X
dc.sourcenlmid: 101596414
dc.subjecthypertrophy
dc.subjectHeart Failure
dc.subjectRna-seq
dc.subjectDilatation
dc.subjectCardiac Recovery
dc.subjectHeart
dc.subjectAnimals
dc.subjectSheep
dc.subjectVentricular Dysfunction, Left
dc.subjectHypertrophy
dc.subjectEchocardiography
dc.titleTranscriptomal Insights of Heart Failure from Normality to Recovery.
dc.typeArticle
dc.date.updated2022-06-29T19:48:47Z
prism.issueIdentifier5
prism.publicationNameBiomolecules
prism.volume12
dc.identifier.doi10.17863/CAM.85985
dcterms.dateAccepted2022-05-13
rioxxterms.versionofrecord10.3390/biom12050731
rioxxterms.versionVoR
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0/
dc.contributor.orcidAl-Mohanna, Futwan [0000-0001-5931-0837]
dc.identifier.eissn2218-273X
cam.issuedOnline2022-05-23


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