Publication Name	World Journal of Diabetes
Manuscript ID	13560
Country	Australia

Received	2014-08-27 17:06
Peer-Review Started	2014-08-28 16:29
To Make the First Decision	2014-12-17 11:20
Return for Revision	2014-12-19 12:10
Revised	2014-12-30 12:54
Second Decision	2015-02-27 09:26
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2015-03-09 16:50
Articles in Press	2015-03-09 16:50
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2015-06-27 16:15
Publish the Manuscript Online	2015-07-10 18:24

ISSN	1948-9358 (online)
Open Access	This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Copyright	© The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
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Category	Physiology
Manuscript Type	Review
Article Title	Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathy
Manuscript Source	Invited Manuscript
All Author List	Mark T Waddingham, Amanda J Edgley, Hirotsugu Tsuchimochi, Darren J Kelly, Mikiyasu Shirai and James T Pearson
Funding Agency and Grant Number	Funding Agency Grant Number International Synchrotron Access Program (AS/IA133) of the Australian Synchrotron to Pearson JT Ministry of Education, Culture, Sports, Sciences and Technology of Japan to Shirai M
Corresponding Author	James T Pearson, PhD, Monash Biomedical Imaging Facility, Monash University, 770 Blackburn Road, Clayton, Victoria 3168, Australia. james.pearson@monash.edu
Key Words	Diabetes; Prediabetes; Insulin resistance; Myocardium; Sarcomere; Protein kinase C; Rho kinase
Core Tip	Pathological changes in cardiac muscle under-lie diabetic cardiomyopathy (DCM) independent of hypertension and atherosclerosis. In advanced diabetes, fibrosis, hypertrophy and apoptosis, reduce myocardial compliance, which leads to increased diastolic filling pressures and overt left ventricular diastolic dysfunction. However, detrimental changes in sarcomeric and other cytoskeletal proteins in the cardiomyocytes of animal models of diabetes precede remodeling of the cardiac extracellular matrix, which has until now been considered the main contributor to diabetic diastolic dysfunction. An important target for preventing early DCM are the protein kinase C/rho-kinase pathways that drive oxidative stress and reduce myosin head cycling and prolong Ca2+ transients.
Publish Date	2015-07-10 18:24
Citation	Waddingham MT, Edgley AJ, Tsuchimochi H, Kelly DJ, Shirai M, Pearson JT. Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathy. World J Diabetes 2015; 6(7): 943-960
URL	http://www.wjgnet.com/1948-9358/full/v6/i7/943.htm
DOI	http://dx.doi.org/10.4239/wjd.v6.i7.943

Full Article (PDF)	WJD-6-943.pdf
Full Article (Word)	WJD-6-943.doc
Manuscript File	13560-Review.doc
Answering Reviewers	13560-Answering reviewers.pdf
Copyright License Agreement	13560-Copyright assignment.pdf
Peer-review Report	13560-Peer-review(s).pdf
Scientific Misconduct Check	13560-Scientific misconduct check.pdf
Scientific Editor Work List	13560-Scientific editor work list.pdf