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©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Cardiol. Jul 26, 2014; 6(7): 577-584
Published online Jul 26, 2014. doi: 10.4330/wjc.v6.i7.577
Published online Jul 26, 2014. doi: 10.4330/wjc.v6.i7.577
Mechanisms underlying the impaired contractility of diabetic cardiomyopathy
Marie-Louise Ward, David J Crossman, Department of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand
Author contributions: Ward ML and Crossman DJ contributed to writing the manuscript; Ward ML drafted the review; Crossman DJ collected and analysed the immunocytochemistry data.
Supported by The Health Research Council of New Zealand
Correspondence to: 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
Telephone: +64-9-9234889 Fax: +64-9-3737499
Received: January 17, 2014
Revised: March 25, 2014
Accepted: April 25, 2014
Published online: July 26, 2014
Revised: March 25, 2014
Accepted: April 25, 2014
Published online: July 26, 2014
Core Tip
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.