© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Subcellular remodeling and heart dysfunction in chronic diabetes
aInstitute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, 351 Tache Avenue, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg R2H 2A6, Canada
bAoto Hospital, Jikei University, Tokyo, Japan
* Corresponding author. Tel.: +204-235-3417; Fax: +204-233-6732; E-mail: cvso@sbrc.umanitoba.ca
Heart dysfunction in chronic diabetes has been observed to be associated with depressed myofibrillar adenosine triphosphatase activities as well as abnormalities in the sarcoplasmic reticular and sarcolemmal calcium transport processes. The evidence has been presented to show that alterations in the expression of myosin isozymes and regulatory proteins as well as myosin phosphorylation contribute to the development of myofibrillar remodeling in the diabetic heart. Defects in sarcoplasmic reticular and sarcolemmal calcium transport appear to be due to the accumulation of lipid metabolites in the membrane. Different agents, such as calcium-antagonists, beta-adrenoceptor blockers, angiotensin converting enzyme inhibitors, metabolic interventions and antioxidants, have been reported to exert beneficial effects in preventing subcellular remodeling and cardiac dysfunction in chronic diabetes. Clinical and experimental investigations have suggested that increased sympathetic activity, activated cardiac renin–angiotensin system, myocardial ischemia/functional hypoxia and elevated levels of glucose for a prolonged period, due to insulin deficiency, result in oxidative stress. It is proposed that oxidative stress associated with a deficit in the status of the antioxidant defense system may play a critical role in subcellular remodeling, calcium-handling abnormalities and subsequent diabetic cardiomyopathy.
KEYWORDS Diabetic cardiomyopathy; Myofibrils; Troponin–tropomyosin; Sarcoplasmic reticulum; Sarcolemma; Antioxidants
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