dc.contributor.author |
Lim, S |
en |
dc.contributor.author |
McMahon, CD |
en |
dc.contributor.author |
Matthews, KG |
en |
dc.contributor.author |
Devlin, GP |
en |
dc.contributor.author |
Elston, Marianne |
en |
dc.contributor.author |
Conaglen, John |
en |
dc.date.accessioned |
2018-10-04T02:58:38Z |
en |
dc.date.issued |
2018-06 |
en |
dc.identifier.citation |
Heart, Lung and Circulation. 27(6),693-701, 2018 |
en |
dc.identifier.issn |
1443-9506 |
en |
dc.identifier.uri |
http://hdl.handle.net/2292/38797 |
en |
dc.description.abstract |
BackgroundMyostatin inhibits the development of skeletal muscle and regulates the proliferation of skeletal muscle fibroblasts. However, the role of myostatin in regulating cardiac muscle or myofibroblasts, specifically in acute myocardial infarction (MI), is less clear. This study sought to determine whether absence of myostatin altered left ventricular function post-MI. MethodsMyostatin-null mice (Mstn−/−) and wild-type (WT) mice underwent ligation of the left anterior descending artery to induce MI. Left ventricular function was measured at baseline, days 1 and 28 post-MI. Immunohistochemistry and immunofluorescence were obtained at day 28 for cellular proliferation, collagen deposition, and myofibroblastic activity. ResultsWhilst left ventricular function at baseline and size of infarct were similar, significant differences in favour of Mstn−/− compared to WT mice post-MI include a greater recovery of ejection fraction (61.8±1.1% vs 57.1±2.3%, p<0.01), less collagen deposition (41.9±2.8% vs 54.7±3.4%, p<0.05), and lower mortality (0 vs. 20%, p<0.05). There was no difference in the number of BrdU positive cells, percentage of apoptotic cardiomyocytes, or size of cardiomyocytes post-MI between WT and Mstn−/− mice. ConclusionsAbsence of myostatin potentially protects the function of the heart post-MI with improved survival, possibly by limiting extent of fibrosis. |
en |
dc.publisher |
Elsevier |
en |
dc.relation.ispartofseries |
Heart, Lung and Circulation |
en |
dc.rights |
Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. |
en |
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
en |
dc.rights.uri |
https://www.elsevier.com/journals/heart-lung-and-circulation/1443-9506/guide-for-authors#13300 |
en |
dc.title |
Absence of myostatin inproves cardiac function following myocardial infarction |
en |
dc.type |
Journal Article |
en |
dc.identifier.doi |
10.1016/j.hlc.2017.05.138 |
en |
pubs.issue |
6 |
en |
pubs.begin-page |
693 |
en |
pubs.volume |
27 |
en |
dc.rights.holder |
Copyright: Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ) |
en |
pubs.author-url |
https://www.sciencedirect.com/science/article/pii/S144395061731260X |
en |
pubs.end-page |
701 |
en |
dc.rights.accessrights |
http://purl.org/eprint/accessRights/OpenAccess |
en |
pubs.subtype |
Article |
en |
pubs.elements-id |
655743 |
en |
pubs.org-id |
Medical and Health Sciences |
en |
pubs.org-id |
School of Medicine |
en |
pubs.org-id |
Medicine Department |
en |
pubs.record-created-at-source-date |
2017-08-31 |
en |
pubs.online-publication-date |
2017-06-15 |
en |