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Molecular regulation of cardiac regeneration post-myocardial infarction /

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dc.contributor.authorLock, Mitchell Clay
dc.contributor.schoolUniversity of South Australia. School of Pharmacy and Medical Sciences.
dc.contributor.schoolSchool of Pharmacy and Medical Sciences.
dc.date.issued2019
dc.description1 ethesis (xxxvi, 267 pages) :
dc.descriptionillustrations (some colour), charts (some colour)
dc.descriptionIncludes bibliographical references.
dc.description.abstractCardiovascular disease is the leading cause of morbidity and mortality worldwide. The fetal heart has the unique ability to regenerate and repair after myocardial infarction (MI) through proliferation of cardiomyocytes. This response is blocked in the adolescent heart. Within this thesis we investigated three possible sources for the different response to damage between fetal and postnatal life (Physiological, Gene, and miRNA response) using a sheep model of MI. We used array experiments to probe thousands of genes and miRNAs to identify possible therapeutic targets of myocardial repair. The results indicate that the fetal heart has a strong resistance to damage, alongside unique modulation of miRNAs involved in proliferation and inflammation. Targeting the uniquely expressed genes and miRNAs identified in this thesis may lead to the development of beneficial treatments for heart attack.
dc.description.dissertationThesis (PhD(Medical Science))--University of South Australia, 2019.
dc.identifier.urihttps://hdl.handle.net/11541.2/139061
dc.language.isoen
dc.provenanceCopyright 2019 Mitchell Clay Lock.
dc.subjectcardiovascular;myocardial infarction;regeneration
dc.subject.lcshFetal heart
dc.subject.lcshHeart
dc.subject.lcshRegenerative medicine.
dc.titleMolecular regulation of cardiac regeneration post-myocardial infarction /
dc.typethesis
dcterms.accessRights506 0#$fstar $2Unrestricted online access
ror.fileinfo12179936070001831 13179936060001831 Lock, Mitchell Clay - Thesis
ror.mmsid9916315905701831

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