Regulation of sarco(endo)plasmic reticulum Ca2+ adenosine triphosphatase by phospholamban and sarcolipin: implication for cardiac hypertrophy and failure

The cardiac isoform of sarco(endo)plasmic reticulum Ca(2)(+) adenosine triphosphatase (SERCA2a) plays an important role in the contraction and relaxation of cardiac muscle. Phospholamban (PLN) and its homologue sarcolipin (SLN) are the endogenous regulators of SERCA2a. Evidence is accumulating that...

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Bibliographic Details
Published in:Trends in cardiovascular medicine 2003-05, Vol.13 (4), p.152-157
Main Authors: Asahi, Michio, Nakayama, Hiroyuki, Tada, Michihiko, Otsu, Kinya
Format: Article
Language:English
Subjects:
Animals
Calcium-Binding Proteins - pharmacology
Calcium-Binding Proteins - physiology
Calcium-Transporting ATPases - physiology
Cardiomegaly - enzymology
Cardiomegaly - physiopathology
Heart Failure - enzymology
Heart Failure - physiopathology
Humans
Muscle Proteins - pharmacology
Muscle Proteins - physiology
Myocardial Contraction - physiology
Proteolipids - pharmacology
Proteolipids - physiology
Sarcoplasmic Reticulum - enzymology
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Summary:The cardiac isoform of sarco(endo)plasmic reticulum Ca(2)(+) adenosine triphosphatase (SERCA2a) plays an important role in the contraction and relaxation of cardiac muscle. Phospholamban (PLN) and its homologue sarcolipin (SLN) are the endogenous regulators of SERCA2a. Evidence is accumulating that SERCA2a is intimately involved in the pathogenesis of cardiac hypertrophy and failure. Recent studies using genetically engineered animals revealed the implication of PLN for the development of cardiomyopathic phenotypes. This review focuses on advances in the understanding of molecular regulation of SERCA2a by PLN and SLN, and their implications for cardiac hypertrophy and failure in vivo.
ISSN:1050-1738
DOI:10.1016/s1050-1738(03)00037-9