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Cardiovascular Research Advance Access [Accepted Manuscript] published online on October 13, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn281
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

Subcellular remodeling may induce cardiac dysfunction in congestive heart failure

Naranjan S. Dhalla, Harjot K. Saini-Chohan, Delfin Rodriguez-Leyva, Vijayan Elimban, Melissa R. Dent and Paramjit S. Tappia

Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada

Correspondence to: Dr. Naranjan S. Dhalla Institute of Cardiovascular Sciences St. Boniface General Hospital Research Centre 351 Tache Avenue Winnipeg, Manitoba, Canada R2H 2A6 Tel: (204) 235-3421 Fax: (204) 233-6723 E-mail: nsdhalla{at}sbrc.ca

It is commonly held that cardiac remodeling, represented by changes in muscle mass, size and shape of the heart, explains the progression of congestive heart failure (CHF). However, this concept does not provide any clear information regarding the development of cardiac dysfunction in CHF. Extensive research has revealed that various subcellular organelles such as extracellular matrix, sarcolemma, sarcoplasmic reticulum, myofibrils, mitochondria and nucleus undergo varying degrees of changes in their biochemical compositions and molecular structure in CHF. This subcellular remodeling occurs due to alterations in cardiac gene expression as well as activation of different proteases and phospholipases in the failing hearts. Several mechanisms including increased ventricular wall stress, prolonged activation of the renin-angiotensin and sympathetic systems and oxidative stress have been suggested to account for subcellular remodeling in CHF. Furthermore, subcellular remodeling is associated with changes in cardiomyocyte structure, cation homeostasis as well as functional activities of cation channels and transporters, receptor-mediated signal transduction, Ca2+-cycling proteins, contractile and regulatory proteins, and energy production system during the development of heart failure. The existing evidence support the view that subcellular remodeling may result in cardiac dysfunction and thus play a critical role in the transition of cardiac hypertrophy to heart failure.

KEYWORDS Cardiac hypertrophy; heart failure; sarcolemmal remodeling; sarcoplasmic reticular remodeling; myofibrillar remodeling; mitochondrial remodeling; extracellular remodeling

Time for primary review: 32 Days


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