dc.contributor.author |
Lim, Sarina |
|
dc.contributor.author |
McMahon, Chris D |
|
dc.contributor.author |
Matthews, Kenneth G |
|
dc.contributor.author |
Devlin, Gerard P |
|
dc.contributor.author |
Elston, Marianne S |
|
dc.contributor.author |
Conaglen, John V |
|
dc.coverage.spatial |
Australia |
|
dc.date.accessioned |
2022-08-15T00:24:15Z |
|
dc.date.available |
2022-08-15T00:24:15Z |
|
dc.date.issued |
2018-06 |
|
dc.identifier.citation |
(2018). Heart Lung and Circulation, 27(6), 693-701. |
|
dc.identifier.issn |
1443-9506 |
|
dc.identifier.uri |
https://hdl.handle.net/2292/60787 |
|
dc.description.abstract |
<h4>Background</h4>Myostatin 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.<h4>Methods</h4>Myostatin-null mice (Mstn<sup>-/-</sup>) 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.<h4>Results</h4>Whilst left ventricular function at baseline and size of infarct were similar, significant differences in favour of Mstn<sup>-/-</sup> 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<sup>-/-</sup> mice.<h4>Conclusions</h4>Absence of myostatin potentially protects the function of the heart post-MI with improved survival, possibly by limiting extent of fibrosis. |
|
dc.format.medium |
Print-Electronic |
|
dc.language |
eng |
|
dc.publisher |
Elsevier |
|
dc.relation.ispartofseries |
Heart, lung & circulation |
|
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. |
|
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
|
dc.rights.uri |
https://creativecommons.org/licenses/by-nc-nd/4.0/ |
|
dc.subject |
Myocardium |
|
dc.subject |
Coronary Vessels |
|
dc.subject |
Heart Ventricles |
|
dc.subject |
Fibroblasts |
|
dc.subject |
Myocytes, Cardiac |
|
dc.subject |
Animals |
|
dc.subject |
Mice, Inbred C57BL |
|
dc.subject |
Mice, Knockout |
|
dc.subject |
Mice |
|
dc.subject |
Myocardial Infarction |
|
dc.subject |
Disease Models, Animal |
|
dc.subject |
Echocardiography |
|
dc.subject |
Immunohistochemistry |
|
dc.subject |
Apoptosis |
|
dc.subject |
Ventricular Function, Left |
|
dc.subject |
Ventricular Remodeling |
|
dc.subject |
Male |
|
dc.subject |
Myostatin |
|
dc.subject |
Ejection fraction |
|
dc.subject |
Fibrosis |
|
dc.subject |
Heart Disease |
|
dc.subject |
Cardiovascular |
|
dc.subject |
Heart Disease - Coronary Heart Disease |
|
dc.subject |
1 Underpinning research |
|
dc.subject |
1.1 Normal biological development and functioning |
|
dc.subject |
3 Good Health and Well Being |
|
dc.subject |
Science & Technology |
|
dc.subject |
Life Sciences & Biomedicine |
|
dc.subject |
Cardiac & Cardiovascular Systems |
|
dc.subject |
Cardiovascular System & Cardiology |
|
dc.subject |
SKELETAL-MUSCLE FIBROSIS |
|
dc.subject |
HEART-FAILURE |
|
dc.subject |
INTERSTITIAL FIBROSIS |
|
dc.subject |
MODEL |
|
dc.subject |
MOUSE |
|
dc.subject |
HYPERTROPHY |
|
dc.subject |
GROWTH |
|
dc.subject |
SIZE |
|
dc.subject |
1102 Cardiorespiratory Medicine and Haematology |
|
dc.subject |
Clinical Medicine and Science |
|
dc.subject |
1117 Public Health and Health Services |
|
dc.title |
Absence of Myostatin Improves Cardiac Function Following Myocardial Infarction. |
|
dc.type |
Journal Article |
|
dc.identifier.doi |
10.1016/j.hlc.2017.05.138 |
|
pubs.issue |
6 |
|
pubs.begin-page |
693 |
|
pubs.volume |
27 |
|
dc.date.updated |
2022-07-21T01:53:14Z |
|
dc.rights.holder |
Copyright: Elsevier |
en |
dc.identifier.pmid |
28690022 (pubmed) |
|
pubs.author-url |
https://www.ncbi.nlm.nih.gov/pubmed/28690022 |
|
pubs.end-page |
701 |
|
pubs.publication-status |
Published |
|
dc.rights.accessrights |
http://purl.org/eprint/accessRights/OpenAccess |
en |
pubs.subtype |
Journal Article |
|
pubs.elements-id |
869781 |
|
pubs.org-id |
Medical and Health Sciences |
|
pubs.org-id |
School of Medicine |
|
pubs.org-id |
Medicine Department |
|
dc.identifier.eissn |
1444-2892 |
|
dc.identifier.pii |
S1443-9506(17)31260-X |
|
pubs.record-created-at-source-date |
2022-07-21 |
|
pubs.online-publication-date |
2018-06 |
|