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Cardiovascular Research Advance Access originally published online on October 30, 2007
Cardiovascular Research 2008 77(2):265-273; doi:10.1093/cvr/cvm056
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

Regulation of sarcoplasmic reticulum Ca2+ ATPase pump expression and its relevance to cardiac muscle physiology and pathology

Muthu Periasamy*, Poornima Bhupathy and Gopal J. Babu*,{dagger}

Department of Physiology and Cell Biology, College of Medicine and Public Health, The Ohio State University, 304 Hamilton Hall, 1645 Neil Ave, Columbus, OH 43210, USA

* Corresponding author. Tel: +1 614 292 2310; fax: +1 614 292 4888. E-mail addresses: periasamy.1{at}osu.edu (M.P.)/ babugo{at}umdnj.edu (G.J.B.)

Cardiac sarcoplasmic reticulum (SR) Ca2+ ATPase (SERCA2a) plays a central role in myocardial contractility. SERCA2a actively transports Ca2+ into the SR and regulates cytosolic Ca2+ concentration, SR Ca2+ load, and the rate of contraction and relaxation of the heart. In the heart, SERCA pump activity is regulated by two small molecular weight proteins: phospholamban (PLB) and sarcolipin (SLN). Decreases in the expression levels of SERCA2a have been observed in a variety of pathological conditions. In addition, altered expression of PLB and SLN has been reported in many cardiac diseases. Thus, SERCA2a is a major regulator of intracellular Ca2+ homeostasis, and changes in the expression and activity of the SERCA pump contribute to the decreased SR Ca2+ content and cardiac dysfunction during pathogenesis. In this review, we discuss the mechanisms controlling SERCA pump expression and activity both during normal physiology and under pathological states.

KEYWORDS Atria; Ventricle; SR Ca2+ ATPase; Phospholamban; Sarcolipin; Calcium; Cardiac contractility

Time for primary review: 39 days

{dagger} Present address. Department of Cell Biology and Molecular Medicine, UMDNJ-NJMS, Newark, NJ 07101, USA.


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