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

Abstract
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.
AuthorsMichio Asahi, Hiroyuki Nakayama, Michihiko Tada, Kinya Otsu
JournalTrends in cardiovascular medicine (Trends Cardiovasc Med) Vol. 13 Issue 4 Pg. 152-7 (May 2003) ISSN: 1050-1738 [Print] United States
PMID12732449 (Publication Type: Journal Article, Review)
Chemical References
  • Calcium-Binding Proteins
  • Muscle Proteins
  • Proteolipids
  • phospholamban
  • sarcolipin
  • Calcium-Transporting ATPases
Topics
  • Animals
  • Calcium-Binding Proteins (pharmacology, physiology)
  • Calcium-Transporting ATPases (physiology)
  • Cardiomegaly (enzymology, physiopathology)
  • Heart Failure (enzymology, physiopathology)
  • Humans
  • Muscle Proteins (pharmacology, physiology)
  • Myocardial Contraction (physiology)
  • Proteolipids (pharmacology, physiology)
  • Sarcoplasmic Reticulum (enzymology)

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