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Cardiovascular Research Advance Access originally published online on October 13, 2008
Cardiovascular Research 2009 81(3):429-438; 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 remodelling 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, 351 Tache Avenue, Winnipeg, Manitoba, Canada R2H 2A6

* Corresponding author. Tel: +1 204 235 3417; fax: +1 204 237-0347. E-mail address: nsdhalla{at}sbrc.ca

It is commonly held that cardiac remodelling, 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 the extracellular matrix, sarcolemma, sarcoplasmic reticulum, myofibrils, mitochondria, and nucleus undergo varying degrees of changes in their biochemical composition and molecular structure in CHF. This subcellular remodelling 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 remodelling in CHF. Furthermore, subcellular remodelling 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 during the development of heart failure. The existing evidence supports the view that subcellular remodelling 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 remodelling; Sarcoplasmic reticular remodelling; Myofibrillar remodelling; Mitochondrial remodelling; Extracellular remodelling

Time for primary review: 32 days


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