Document Detail

Downregulation of Ca2+ signalling proteins in cardiac hypertrophy.
MedLine Citation:
PMID:  20440249     Owner:  NLM     Status:  MEDLINE    
Calcium (Ca2+) signaling plays an essential role in several functions of cardiac myocytes. Transient rises and reductions of cytosolic Ca2+, permitted by the sarcoplasmic reticulum Ca2+ ATPase and other proteins, control each cycle of contraction and relaxation. Prolonged rises of cytosolic Ca2+ are involved in transcriptional activation, including the hypertrophy program. Furthermore, activation of transcriptional pathways produced by excitation of membrane receptors and involving Protein Kinases C and D, calcineurin, mitogen-activated protein kinases and glycogen synthase kinase 3b, generate competitive recruitment of transcriptional factors whereby Ca2+ signaling proteins are downregulated in cardiac hypertrophy. This imbalance leads to defects of muscle contraction (i.e., systole) and relaxation (i.e., diastole), and ultimately cardiac failure. Extensive experimentation on gene transfer and gene deletion is under way to clarify the role of Ca2+ signaling proteins in cardiac hypertrophy and failure, and to evaluate the possibility of gene therapy. On the other hand, the need for pharmacological agents directed to function or transcription/expression of Ca2+ signaling proteins is emphasized, considering their easier delivery and wide population targeting.
A M Prasad; G Inesi
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Minerva cardioangiologica     Volume:  58     ISSN:  0026-4725     ISO Abbreviation:  Minerva Cardioangiol     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-05-04     Completed Date:  2010-09-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0400725     Medline TA:  Minerva Cardioangiol     Country:  Italy    
Other Details:
Languages:  eng     Pagination:  193-204     Citation Subset:  IM    
California Pacific Medical Center, Research Institute, San Francisco, CA, USA.
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MeSH Terms
Calcium Signaling / physiology*
Cardiomegaly / drug therapy,  metabolism*
Intracellular Signaling Peptides and Proteins / physiology
Grant Support
Reg. No./Substance:
0/Intracellular Signaling Peptides and Proteins

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