Altered intracellular Ca2+ handling in heart failure.

Abstract

Structural and functional alterations in the Ca2+ regulatory proteins present in the sarcoplasmic reticulum have recently been shown to be strongly involved in the pathogenesis of heart failure. Chronic activation of the sympathetic nervous system or of the renin-angiotensin system induces abnormalities in both the function and structure of these proteins. We review here the considerable body of evidence that has accumulated to support the notion that such abnormalities contribute to a defectiveness of contractile performance and hence to the progression of heart failure.

• Authors: Masafumi Yano, Yasuhiro Ikeda, Masunori Matsuzaki
• Journal: The Journal of clinical investigation (J Clin Invest) Vol. 115 Issue 3 Pg. 556-64 (Mar 2005) ISSN: 0021-9738 [Print] United States
• PMID: 15765137 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Calcium-Binding Proteins
• Muscle Proteins
• Ryanodine Receptor Calcium Release Channel
• Calcium

Topics

• Animals
• Calcium (metabolism)
• Calcium Signaling (physiology)
• Calcium-Binding Proteins (genetics, metabolism)
• Cardiac Output, Low (genetics, metabolism, physiopathology, therapy)
• Cardiomyopathy, Hypertrophic (genetics, metabolism, pathology)
• Humans
• Muscle Proteins (metabolism)
• Myocardial Contraction (physiology)
• Myocytes, Cardiac (cytology, metabolism)
• Ryanodine Receptor Calcium Release Channel (chemistry, genetics, metabolism)
• Sarcoplasmic Reticulum (metabolism)