Skip Navigation



Cardiovascular Research Advance Access [Accepted Manuscript] published online on October 30, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm056
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
77/2/265    most recent
cvm056v2
cvm056v1
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Periasamy, M.
Right arrow Articles by Babu, G. J
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Periasamy, M.
Right arrow Articles by Babu, G. J
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

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*,¶

Department of Physiology and Cell Biology The Ohio State University, Columbus OH, 43210

* Corresponding author: Dr. Muthu Periasamy (periasamy.1{at}osu.edu) or Dr. Gopal J Babu (babugo{at}umdnj.edu), Department of Physiology and Cell Biology, 304 Hamilton Hall, 1645 Neil Ave, The Ohio State University Medical Center, Columbus, OH 43210 Tel: 614-292-2310; Fax: 614-292-4888

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

Present address: Department of Cell Biology and Molecular Medicine, UMDNJ-NJMS, Newark, NJ 07101


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
I. Vandecaetsbeek, M. Trekels, M. De Maeyer, H. Ceulemans, E. Lescrinier, L. Raeymaekers, F. Wuytack, and P. Vangheluwe
Structural basis for the high Ca2+ affinity of the ubiquitous SERCA2b Ca2+ pump
PNAS, November 3, 2009; 106(44): 18533 - 18538.
[Abstract] [Full Text] [PDF]

Home page
 Phil Trans R Soc AHome page
J. T. Koivumaki, J. Takalo, T. Korhonen, P. Tavi, and M. Weckstrom
Modelling sarcoplasmic reticulum calcium ATPase and its regulation in cardiac myocytes
Phil Trans R Soc A, June 13, 2009; 367(1896): 2181 - 2202.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
D. Garcia-Dorado, H. M. Piper, and D. A. Eisner
Sarcoplasmic reticulum and mitochondria in cardiac pathophysiology
Cardiovasc Res, January 15, 2008; 77(2): 231 - 233.
[Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.