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8/22/2014 2:47:00 PM | Browse: 907 | Download: 739
Publication Name World Journal of Cardiology
Manuscript ID 9043
Country New Zealand
Received
2014-01-17 09:17
Peer-Review Started
2014-01-17 15:11
To Make the First Decision
2014-03-12 17:00
Return for Revision
2014-03-19 14:45
Revised
2014-03-25 02:54
Second Decision
2014-04-29 08:24
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief
2014-04-29 08:38
Articles in Press
2014-05-23 09:00
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript
2014-07-17 13:46
Publish the Manuscript Online
2014-08-20 20:27
ISSN 1949-8462 (online)
Open Access
Copyright
Article Reprints For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
Permissions For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
Publisher Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Website http://www.wjgnet.com
Category Cardiac & Cardiovascular Systems
Manuscript Type Topic Highlights
Article Title Mechanisms underlying the impaired contractility of diabetic cardiomyopathy
Manuscript Source Invited Manuscript
All Author List Marie-Louise Ward and David J Crossman
Funding Agency and Grant Number
Funding Agency Grant Number
Health Research Council of New Zealand
Corresponding Author Marie-Louise Ward, PhD, Department of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland 1023, New Zealand. m.ward@auckland.ac.nz
Key Words Diabetic cardiomyopathy; Heart failure; Contractility; T-tubules; Excitation-contraction coupling; Calcium homeostasis
Core Tip Diabetic patients develop a cardiomyopathy that is independent of vascular disease, and is thought to develop as a direct result of the prolonged hyperglycaemia. Animal models of diabetes can help us understand the cellular mechanisms that lead ultimately to contractile dysfunction of diabetic cardiomyopathy. The streptozotocin rat model of type 1 diabetes has slowed Ca2+ transients and twitch force kinetics, with reduced myofilament Ca2+ sensitivity. Myocytes are decreased in volume in diabetic hearts, with reduced and disrupted F-actin, and type 1 collagen is increased. Together, these changes all contribute to the reduced contractility of diabetic cardiomyopathy.
Publish Date 2014-08-20 20:27
Citation Ward ML, Crossman DJ. Mechanisms underlying the impaired contractility of diabetic cardiomyopathy. World J Cardiol 2014; 6(7): 577-584
URL http://www.wjgnet.com/1949-8462/full/v6/i7/577.htm
DOI http://dx.doi.org/10.4330/wjc.v6.i7.577
Full Article (PDF) WJC-6-577.pdf
Full Article (Word) WJC-6-577.doc
Manuscript File 9043-Review.docx
Answering Reviewers 9043-Answering reviewers.pdf
Copyright License Agreement 9043-Copyright assignment.pdf
Peer-review Report 9043-Peer review(s).pdf
Scientific Editor Work List 9043-Scientific editor work list.doc